Human Parasites

  • HELMINTHS

    HELMINTHS: STRUCTURE, CLASSIFICATION, GROWTH, DEVELOPMENT, PATHOGENESIS, AND DEFENSES

    General Concepts

    The helminths are worm-like parasites. The clinically relevant groups are separated according to their general external shape and the host organ they inhabit. There are both hermaphroditic and bisexual species. The definitive classification is based on the external and internal morphology of egg, larval, and adult stages.

    Flukes (Trematodes)

    Adult flukes are leaf-shaped flatworms. Prominent oral and ventral suckers help maintain position in situ. Flukes are hermaphroditic except for blood flukes, which are bisexual. The life-cycle includes a snail intermediate host.

    Tapeworms (Cestodes)

    Adult tapeworms are elongated, segmented, hermaphroditic flatworms that inhabit the intestinal lumen. Larval forms, which are cystic or solid, inhabit extraintestinal tissues.

    Roundworms (Nematodes)

    Adult and larval roundworms are bisexual, cylindrical worms. They inhabit intestinal and extraintestinal sites.

    Classification

    Helminth is a general term for a parasitic worm. The helminths include the Platyhelminthes or flatworms (flukes and tapeworms) and the Nematoda or roundworms.

    Characteristics

    All helminths are relatively large (> 1 mm long); some are very large (> 1 m long). All have well-developed organ systems and most are active feeders. The body is either flattened and covered with plasma membrane (flatworms) or cylindrical and covered with cuticle (roundworms). Some helminths are hermaphrodites; others have separate sexes.

    Epidemiology

    Helminths are worldwide in distribution; infection is most common and most serious in poor countries. The distribution of these diseases is determined by climate, hygiene, diet, and exposure to vectors.

    Infection

    The mode of transmission varies with the type of worm; it may involve ingestion of eggs or larvae, penetration by larvae, bite of vectors, or ingestion of stages in the meat of intermediate hosts. Worms are often long-lived.

    Pathogenesis

    Many infections are asymptomatic; pathologic manifestations depend on the size, activity, and metabolism of the worms. Immune and inflammatory responses also cause pathology.

    Host Defenses

    Nonspecific defense mechanisms limit susceptibility. Antibody- and cell-mediated responses are important, as is inflammation. Parasites survive defenses through many evasion strategies.

    Introduction

    Helminth is a general term meaning worm. The helminths are invertebrates characterized by elongated, flat or round bodies. In medically oriented schemes the flatworms or platyhelminths (platy from the Greek root meaning “flat”) include flukes and tapeworms. Roundworms are nematodes (nemato from the Greek root meaning “thread”). These groups are subdivided for convenience according to the host organ in which they reside, e.g., lung flukes, extraintestinal tapeworms, and intestinal roundworms. This chapter deals with the structure and development of the three major groups of helminths.

    Helminths develop through egg, larval (juvenile), and adult stages. Knowledge of the different stages in relation to their growth and development is the basis for understanding the epidemiology and pathogenesis of helminth diseases, as well as for the diagnosis and treatment of patients harboring these parasites.

    Platyhelminths and nematodes that infect humans have similar anatomic features that reflect common physiologic requirements and functions. The outer covering of helminths is the cuticle or tegument. Prominent external structures of flukes and cestodes are acetabula (suckers) or bothria (false suckers). Male nematodes of several species possess accessory sex organs that are external modifications of the cuticle. Internally, the alimentary, excretory, and reproductive systems can be identified by an experienced observer. Tapeworms are unique in lacking an alimentary canal. This lack means that nutrients must be absorbed through the tegument. The blood flukes and nematodes are bisexual. All other flukes and tapeworm species that infect humans are hermaphroditic.

    With few exceptions, adult flukes, cestodes, and nematodes produce eggs that are passed in excretions or secretions of the host. The various stages and their unique characteristics will be reviewed in more detail as each major group of helminths is considered.

    Helminths - worms - are some of the world's commonest parasites (see Ch. 86). They belong to two major groups of animals, the flatworms or Platyhelminthes (flukes and tapeworms) and the roundworms or Nematoda. All are relatively large and some are very large, exceeding one meter in length.

    Their bodies have well-developed organ systems, especially reproductive organs, and most helminths are active feeders. The bodies of flatworms are flattened and covered by a plasma membrane, whereas roundworms are cylindrical and covered by a tough cuticle. Flatworms are usually hermaphroditic whereas roundworms have separate sexes; both have an immense reproductive capacity.

    The most serious helminth infections are acquired in poor tropical and subtropical areas, but some also occur in the developed world; other, less serious, infections are worldwide in distribution. Exposure to infection is influenced by climate, hygiene, food preferences, and contact with vectors. Many potential infections are eliminated by host defenses; others become established and may persist for prolonged periods, even years. Although infections are often asymptomatic, severe pathology can occur. Because worms are large and often migrate through the body, they can damage the host's tissues directly by their activity or metabolism. Damage also occurs indirectly as a result of host defense mechanisms. Almost all organ systems can be affected.

    Host defense can act through nonspecific mechanisms of resistance and through specific immune responses. Antibody-mediated, cellular, and inflammatory mechanisms all contribute to resistance. However, many worms successfully avoid host defenses in a variety of ways, and can survive in the face of otherwise effective host responses.

    Flukes (Trematodes)

    A dorsoventrally flattened body, bilateral symmetry, and a definite anterior end are features of platyhelminths in general and of trematodes specifically. Flukes are leaf-shaped, ranging in length from a few millimeters to 7 to 8 cm. The tegument is morphologically and physiologically complex. Flukes possess an oral sucker around the mouth and a ventral sucker or acetabulum that can be used to adhere to host tissues. A body cavity is lacking. Organs are embedded in specialized connective tissue or parenchyma. Layers of somatic muscle permeate the parenchyma and attach to the tegument.

    Flukes have a well-developed alimentary canal with a muscular pharynx and esophagus. The intestine is usually a branched tube (secondary and tertiary branches may be present) consisting of a single layer of epithelial cells. The main branches may end blindly or open into an excretory vesicle. The excretory vesicle also accepts the two main lateral collecting ducts of the excretory system, which is of a protonephridial type with flame cells. A flame cell is a hollow, terminal excretory cell that contains a beating (flamelike) group of cilia. These cells, anchored in the parenchyma, direct tissue filtrate through canals into the two main collecting ducts.

    Except for the blood flukes, trematodes are hermaphroditic, having both male and female reproductive organs in the same individual. The male organ consists usually of two testes with accessory glands and ducts leading to a cirrus, or penis equivalent, that extends into the common genital atrium. The female gonad consists of a single ovary with a seminal receptacle and vitellaria, or yolk glands, that connect with the oviduct as it expands into an ootype. The tubular uterus extends from the ootype and opens into the genital atrium. Both self- and cross-fertilization occur. The components of the egg are assembled in the ootype. Eggs pass through the uterus into the genital atrium and exit ventrally through the genital pore. Fluke eggs, except for those of schistosomes, are operculated (have a lid).

    The blood flukes or schistosomes are the only bisexual flukes that infect humans. Although the sexes are separate, the general body structure is the same as that of hermaphroditic flukes. Within the definitive host, the male and female worms inhabit the lumen of blood vessels and are found in close physical association. The female lies within a tegumental fold, the gynecophoral canal, on the ventral surface of the male. The medically important flukes belong to the taxonomic category Digenea. This group of flukes has a developmental cycle requiring at least two hosts, one being a snail intermediate host. Depending on the species, other intermediate hosts may be involved to perpetuate the larval form that infects the definitive human host.

    Flukes go through several larval stages, each with a specific name, before reaching adulthood. Taking into account variations among species, a generalized life cycle of digenetic flukes runs the following course. Eggs are passed in the feces, urine, or sputum of humans and reach an aquatic environment. The eggs hatch, releasing ciliated larvae, or miracidia, which either penetrate or are eaten by a snail intermediate host. In rare instances land snails may serve as intermediate hosts. A saclike sporocyst or redia stage develops from a miracidium within the tissues of the snail.

    The sporocyst gives rise either to rediae or to a daughter sporocyst stage. In turn, from the redia or daughter sporocyst, cercariae develop asexually and migrate out of the snail tissues to the external environment, which is usually aquatic.

    The cercariae, which may possess a tail for swimming, develop further in one of three ways. They either penetrate the definitive host and transform directly into adults, or penetrate a second intermediate host and develop as encysted metacercariae, or they encyst on a substrate, such as vegetation, and develop there as metacercariae. When a metacercarial cyst is ingested, digestion of the cyst liberates an immature fluke that migrates to a specific organ site and develops into an adult worm.

    Tapeworms (Cestodes)

    As members of the platyhelminths, the cestodes, or tapeworms, possess many basic structural characteristics of flukes, but also show striking differences.

    Whereas flukes are flattened and generally leaf-shaped, adult tapeworms are flattened, elongated, and consist of segments called proglottids. Tapeworms vary in length from 2 to 3 mm to 10 m, and may have three to several thousand segments.

    Anatomically, cestodes are divided into a scolex, or head, which bears the organs of attachment, a neck that is the region of segment proliferation, and a chain of proglottids called the strobila. The strobila elongates as new proglottids form in the neck region. The segments nearest the neck are immature (sex organs not fully developed) and those more posterior are mature. The terminal segments are gravid, with the egg-filled uterus as the most prominent feature.

    The scolex contains the cephalic ganglion, or “brain,” of the tapeworm nervous system. Externally, the scolex is characterized by holdfast organs. Depending on the species, these organs consist of a rostellum, bothria, or acetabula. A rostellum is a retractable, conelike structure that is located on the anterior end of the scolex, and in some species is armed with hooks. Bothria are long, narrow, weakly muscular grooves that are characteristic of the pseudophyllidean tapeworms. Acetabula (suckers like those of digenetic trematodes) are characteristic of cyclophyllidean tapeworms.

    A characteristic feature of adult tapeworm is the absence of an alimentary canal, which is intriguing since all of these adult worms inhabit the small intestine. The lack of an alimentary tract means that substances enter the tapeworm across the tegument. This structure is well adapted for transport functions, since it is covered with numerous microvilli resembling those lining the lumen of the mammalian intestine. The excretory system is of the flame cell type.

    Cestodes are hermaphroditic, each proglottid possessing male and female reproductive systems similar to those of digenetic flukes. However, tapeworms differ from flukes in the mechanism of egg deposition. Eggs of pseudophyllidean tapeworms exit through a uterine pore in the center of the ventral surface rather than through a genital atrium, as in flukes. In cyclophyllidean tapeworms, the female system includes a uterus without a uterine pore. Thus, the cyclophyllidean eggs are released only when the tapeworms shed gravid proglottids into the intestine. Some proglottids disintegrate, releasing eggs that are voided in the feces, whereas other proglottids are passed intact.

    The eggs of pseudophyllidean tapeworms are operculated, but those of cyclophyllidean species are not. Eggs of all tapeworms, however, contain at some stage of development an embryo or oncosphere. The oncosphere of pseudophyllidean tapeworms is ciliated externally and is called a coracidium. The coracidium develops into a procercoid stage in its micro-crustacean first immediate host and then into a plerocercoid larva in its next intermediate host which is a vertebrate. The plerocercoid larva develops into an adult worm in the definitive (final) host. The oncosphere of cyclophyllidean tapeworms, depending on the species, develops into a cysticercus larva, cysticercoid larva, coenurus larva, or hydatid larva (cyst) in specific intermediate hosts. These larvae, in turn, become adults in the definitive host.

    Roundworms (Nematodes)

    In contrast to platyhelminths, nematodes are cylindrical rather than flattened; hence the common name roundworm. The body wall is composed of an outer cuticle that has a noncellular, chemically complex structure, a thin hypodermis, and musculature. The cuticle in some species has longitudinal ridges called alae. The bursa, a flaplike extension of the cuticle on the posterior end of some species of male nematodes, is used to grasp the female during copulation.

    The cellular hypodermis bulges into the body cavity or pseudocoelom to form four longitudinal cords—a dorsal, a ventral, and two lateral cords—which may be seen on the surface as lateral lines. Nuclei of the hypodermis are located in the region of the cords. The somatic musculature lying beneath the hypodermis is a single layer of smooth muscle cells. When viewed in cross-section, this layer can be seen to be separated into four zones by the hypodermal cords. The musculature is innervated by extensions of muscle cells to nerve trunks running anteriorly and posteriorly from ganglion cells that ring the midportion of the esophagus.

    The space between the muscle layer and viscera is the pseudocoelom, which lacks a mesothelium lining. This cavity contains fluid and two to six fixed cells (celomocytes) which are usually associated with the longitudinal cords. The function of these cells is unknown.

    The alimentary canal of roundworms is complete, with both mouth and anus. The mouth is surrounded by lips bearing sensory papillae (bristles). The esophagus, a conspicuous feature of nematodes, is a muscular structure that pumps food into the intestine; it differs in shape in different species.

    The intestine is a tubular structure composed of a single layer of columnar cells possessing prominent microvilli on their luminal surface.

    The excretory system of some nematodes consists of an excretory gland and a pore located ventrally in the mid-esophageal region. In other nematodes this structure is drawn into extensions that give rise to the more complex tubular excretory system, which is usually H-shaped, with two anterior limbs and two posterior limbs located in the lateral cords. The gland cells and tubes are thought to serve as absorptive bodies, collecting wastes from the pseudocoelom, and to function in osmoregulation.

    Nematodes are usually bisexual. Males are usually smaller than females, have a curved posterior end, and possess (in some species) copulatory structures, such as spicules (usually two), a bursa, or both. The males have one or (in a few cases) two testes, which lie at the free end of a convoluted or recurved tube leading into a seminal vesicle and eventually into the cloaca.

    The female system is tubular also, and usually is made up of reflexed ovaries. Each ovary is continuous, with an oviduct and tubular uterus. The uteri join to form the vagina, which in turn opens to the exterior through the vulva.

    Copulation between a female and a male nematode is necessary for fertilization except in the genus Strongyloides, in which parthenogenetic development occurs (i.e., the development of an unfertilized egg into a new individual). Some evidence indicates that sex attractants (pheromones) play a role in heterosexual mating. During copulation, sperm is transferred into the vulva of the female. The sperm enters the ovum and a fertilization membrane is secreted by the zygote. This membrane gradually thickens to form the chitinous shell. A second membrane, below the shell, makes the egg impervious to essentially all substances except carbon dioxide and oxygen. In some species, a third proteinaceous membrane is secreted as the egg passes down the uterus by the uterine wall and is deposited outside the shell. Most nematodes that are parasitic in humans lay eggs that, when voided, contain either an uncleaved zygote, a group of blastomeres, or a completely formed larva. Some nematodes, such as the filariae and Trichinella spiralis, produce larvae that are deposited in host tissues.

    The developmental process in nematodes involves egg, larval, and adult stages. Each of four larval stages is followed by a molt in which the cuticle is shed. The larvae are called second-stage larvae after the first molt, and so on.

    Infection

    Transmission of Infection

    Helminths are transmitted to humans in many different ways. The simplest is by accidental ingestion of infective eggs (Ascaris, Echinococcus, Enterobius, Trichuris) or larvae (some hookworms). Other worms have larvae that actively penetrate the skin (hookworms, schistosomes, Strongyloides). In several cases, infection requires an intermediate host vector. In some cases the intermediate vector transmits infective stages when it bites the host to take a blood meal (the arthropod vectors of filarial worms); in other cases, the larvae are contained in the tissues of the intermediate host and are taken in when a human eats that host (Clonorchis in fish, tapeworms in meat and fish, Trichinella in meat). The levels of infection in humans therefore depend on standards of hygiene (as eggs and larvae are often passed in urine or feces), on the climate (which may favor survival of infective stages), on the ways in which food is prepared, and on the degree of exposure to insect vectors.

    Host Factors Influencing Susceptibility

    Human behavior is a major factor influencing susceptibility to infection. If the infective stages of helminths are present in the environment, then certain ways of behaving, particularly with regard to hygiene and food, will result in greater exposure. Because helminths, with few exceptions (Strongyloides, Trichinella, some tapeworm larvae), do not increase their numbers by replication within the same host, the level of infection is directly related to the number of infective stages encountered. Obviously, not every exposure results in the development of a mature infection. Many infective organisms are killed by the host's nonspecific defense mechanisms. Of those that do become established, many are destroyed or eliminated by specific defenses. The number of worms present at any one time therefore represents a dynamic balance between the rate of infection and the efficiency of defense. This balance (which reflects the host's overall susceptibility) is altered by changes in the host's behavior and ability to express forms of defense. Children are more susceptible to many helminths than are adults, and frequently are the most heavily infected members of a community. The waning of immune competence with age may also result in increased levels of infection. Individuals differ genetically in their ability to resist infection, and it is well known that in infected populations, some individuals are predisposed to heavier infections than others. Changes in diet may affect susceptibility, as do the hormonal-immune changes accompanying pregnancy and lactation. An important cause of increased susceptibility is the immune suppression that accompanies concurrent infections with some other pathogens and the development of certain tumors. Similarly, immunosuppressive therapies (irradiation, immunosuppressant drugs) may enhance susceptibility to helminth infection. A particular hazard in immunocompromised patients is the development of disseminated strongyloidiasis, in which large numbers of larvae develop in the body by autoinfection from relatively small numbers of adult Strongyloides stercoralis. It is interesting that the human immunodeficiency virus does not result in an overall increase in susceptibility to helminth infection.

    Parasite Factors Influencing Susceptibility

    The ability of hosts to control infection is offset by the ability of parasites to avoid the host's defenses and increase their survival. In addition to their ability to evade specific immune defenses (see below), many worms are unaffected by the host's attempts to limit their activities or to destroy them simply because they are large and mobile. Many important species measure several centimeters in length or diameter (Ascaris, hookworms, hydatid cysts, Trichuris) and others may exceed one meter in length (tapeworms). Size alone renders many defense mechanisms inoperative, as does the tough cuticle of adult roundworms. The ability of worms to move actively through tissues enables them to escape inflammatory foci.

    Many of the pathogenic consequences of worm infections are related to the size, movement and longevity of the parasites, as the host is exposed to long-term damage and immune stimulation, as well as to the sheer physical consequences of being inhabited by large foreign bodies.

    Pathogenesis
    Direct Damage from Worm Activity

    The most obvious forms of direct damage are those resulting from the blockage of internal organs or from the effects of pressure exerted by growing parasites. Large Ascaris or tapeworms can physically block the intestine, and this may occur after some forms of chemotherapy; migrating Ascaris may also block the bile duct. Granulomas that form around schistosome eggs may block the flow of blood through the liver, and this may lead to pathological changes in that organ and elsewhere. Blockage of lymph flow, leading to elephantiasis, is associated with the presence of adult Wuchereria in lymphatics. Pressure atrophy is characteristic of larval tapeworm infections (hydatid cyst, the larva of Echinococcus granulosus) where the parasite grows as a large fluid-filled cyst in the liver, brain, lungs, or body cavity. The multilocular hydatid cysts caused by Echinococcus multilocularis have a different growth form, metastasizing within organs and causing necrosis. The larvae of Taenia solium, the pork tapeworm, frequently develop in the central nervous system (CNS) and eyes. Some of the neurological symptoms of the resulting condition, called cysticercosis, are caused by the pressure exerted by the cysts.

    Intestinal worms cause a variety of pathologic changes in the mucosa, some reflecting physical and chemical damage to the tissues, others resulting from immunopathologic responses. Hookworms (Ancylostoma and Necator) actively suck blood from mucosal capillaries. The anticoagulants secreted by the worms cause the wounds to bleed for prolonged periods, resulting in considerable blood loss. Heavy infections in malnourished hosts are associated with anemia and protein loss. Protein-losing enteropathies may also result from the inflammatory changes induced by other intestinal worms. Diversion of host nutrients by competition from worms is probably unimportant, but interference with normal digestion and absorption may well aggravate undernutrition. The tapeworm Diphyllobothrium latum can cause vitamin B12 deficiency through direct absorption of this factor.

    Many helminths undertake extensive migrations through body tissues, which both damage tissues directly and initiate hypersensitivity reactions. The skin, lungs, liver, and intestines are the organs most affected. Petechial hemorrhages, pneumonitis, eosinophilia, urticaria and pruritus, organomegaly, and granulomatous lesions are among the signs and symptoms produced during these migratory phases.

    Feeding by worms upon host tissues is an important cause of pathology, particularly when it induces hyperplastic and metaplastic changes in epithelia. For example, liver fluke infections lead to hyperplasia of the bile duct epithelium. Chronic inflammatory changes around parasites (for example, the granulomas around schistosome eggs in the bladder wall) have been linked with neoplasia, but the nature of the link is not known. The continuous release by living worms of excretory-secretory materials, many of which are known to have direct effects upon host cells and tissues, may also contribute to pathology.

    Indirect Damage from Host Response

    As with all infectious organisms, it is impossible to separate the pathogenic effects caused strictly by mechanical or chemical tissue damage from those caused by the immune response to the parasite. All helminths are “foreign bodies” not only in the sense of being large and invasive but also in the immunologic sense: they are antigenic and therefore stimulate immunity. An excellent illustration of this interrelation between direct and indirect damage is seen in the pathology associated with schistosome infections, especially with Schistosoma mansoni. Hypersensitivity- based,granulomatous responses to eggs trapped in the liver cause a physical obstruction to blood flow, which leads to liver pathology. Hypersensitivity-based inflammatory changes probably also contribute to the lymphatic blockage associated with filarial infections (Brugia, Wuchereria).

    Immune-mediated inflammatory changes occur in the skin, lungs, liver, intestine, CNS, and eyes as worms migrate through these structures. Systemic changes such as eosinophilia, edema, and joint pain reflect local allergic responses to parasites. The pathologic consequences of immune-mediated inflammation are seen clearly in intestinal infections (especially Strongyloides and Trichinella infections). Structural changes, such as villous atrophy, develop. The permeability of the mucosa changes, fluid accumulates in the gut lumen, and intestinal transit time is reduced. Prolonged changes of this type may lead to a protein-losing enteropathy. The inflammatory changes that accompany the passage of schistosome eggs through the intestinal wall also cause severe intestinal pathology. Heavy infections with the whipworm Trichuris in the large bowel can lead to inflammatory changes, resulting in blood loss and rectal prolapse.

    The severity of these indirect changes is a result of the chronic nature of the infection. The fact that many worms are extremely long-lived means that many inflammatory changes become irreversible, producing functional changes in tissues. Three examples are the hyperplasia of bile ducts in long-term liver fluke infections, the extensive fibrosis associated with chronic schistosomiasis, and the skin atrophy associated with onchocerciasis. Severe pathology may also result when worms stray into abnormal body sites.

    Defenses Against Infection
    Nonspecific Resistance

    Infective stages attempting to enter via the mouth or through the skin are opposed by the same non-specific defenses that protect humans from invasion of other pathogens. Following oral ingestion, parasites must survive passage through the acid stomach to reach the small bowel. The natural parasites of humans are adapted to do this, but opportunistic parasites may be killed. Similarly, natural parasites are adapted to the environmental conditions of the bowel (and in many cases require them as cues for development), but accidental parasites may find them inappropriate. Penetration into the intestinal wall may trigger inflammatory responses that immobilize and kill the worm. This may itself lead to serious pathology (as in Anisakis infection). Worms entering through the skin must survive the skin secretions, penetrate the epidermal layers, and avoid inflammatory trapping in the dermis. Invasion of humans by the larvae of dog and cat hookworms (Ancylostoma spp.) results in dermatitis and “creeping eruption” as the worms become the focus of inflammatory reactions that form trails in the skin.

    Once in the tissues, worms need the correct sequence of environmental signals to mature. Absent or incomplete signals constitute a form of nonspecific resistance that may partially or completely prevent further development. The parasite may not die, however; indeed, prolonged survival at a larval stage may result in pathology from the continuing inflammatory response (e.g. Toxocara infection).

    Specific Acquired Immunity

    There is no doubt that specific immunity is responsible for the most effective forms of host defense, although the dividing line between nonspecific and specific mechanisms is difficult to draw with precision. All helminths stimulate strong immune responses, which can easily be detected by measuring specific antibody or cellular immunity. Although these responses are useful for diagnosing infection, they frequently appear not to be protective. The high prevalence of helminth infection in endemic areas (sometimes approaching 100 per cent), and the fact that individuals may remain infected for many years and can easily be reinfected after they are cured by chemotherapy, suggest that protective immunity against helminths is weak or absent in humans. However, some degree of immunity does appear to operate, because the intensity of infection often declines with age, and many individuals in endemic areas remain parasitologically negative and/or clinically normal. Evidence from laboratory studies provides some clues as to the mechanisms involved. Antibodies that bind to surface antigens may focus complement- or cell-mediated effectors that can damage the worm. Macrophages and eosinophils are the prime cytotoxic effector cells, and IgM, IgG and IgE are the important immunoglobulins. Antibodies may also block enzymes released by the worm, thus interfering with its ability to penetrate tissues or to feed. Inflammatory changes may concentrate effector cells around worms, and the release of cellular mediators may then disable and kill the worm. Encapsulation of trapped worms by inflammatory cells may also result in the death of the worm, although this is not always the case. Intestinal worms can be dislodged by the structural and physiologic changes that occur in the intestine during acute inflammation. It has long been suspected that IgE-mediated hypersensitivity reactions, involving mast cells and basophils, contribute to this process, but the evidence is still circumstantial. Despite the abundance of IgA in the intestinal lumen, there is no conclusive evidence that it is involved in protective immunity in humans, although some field and laboratory data suggest it is.

    Avoidance of Host Defenses

    Despite their immunogenicity, many helminths survive for extended periods in the bodies of their hosts. Some of the reasons have already been mentioned (size, motility), but we now know that worms employ many sophisticated devices to render host defenses ineffective. Some worms (schistosomes) disguise their outer surface by acquiring host molecules which reduce their antigenicity; intrinsic membrane changes also make these worms resistant to immune attack. Filarial nematodes acquire serum albumin on their cuticle, which may act as a disguise. Many worms release substances that depress lymphocyte function, inactivate macrophages, or digest antibodies. Larval cestodes appear to prolong their survival by producing anticomplement factors which protect their outer layers from lytic attack. Antigenic variation in the strict sense is not known to occur, but many species show a stage-specific change of antigens as they develop, and this phenomenon may delay the development of effective immune mechanisms. All helminths release relatively large amounts of antigenic materials, and this voluminous production may divert immune responses or even locally exhaust immune potential. Irrelevant antibodies produced by the host may block the activity of potentially protective antibodies, as has been shown to be the case in schistosome infections.

    It is striking that many helminth infections are associated with a degree of immune suppression, which may affect specific or general responsiveness. Many explanations have been proposed for this immune suppression, including antigen overload, antigenic competition, induction of suppressor cells, and production of lymphocyte-specific suppressor factors. Reduced immune responsiveness may not only prolong the survival of the original infecting worm species but increase the host's susceptibility to other pathogens. Epidemiologic evidence also raises the possibility that infections acquired early in life—before or shortly after birth—may induce a form of immune tolerance, allowing heavy worm burdens to accumulate in the body.

    The subtlety with which parasitic worms manipulate the host's immune system not only increases their importance as pathogens but also creates formidable problems for their control and eradication.

    For more information view the source: Medical Microbiology

  • ANCYLOSTOMA NECATOR

    An estimated 576-740 million people in the world are infected with  hookworm. Hookworm was once widespread in the United States, particularly in the southeastern region, but improvements in living conditions have greatly reduced hookworm infections. Hookworm, Ascaris, and whipworm are known as soil-transmitted helminths (parasitic worms). Together, they account for a major burden of  disease worldwide.

    Hookworms live  in the small intestine. Hookworm eggs are  passed in the feces of an infected person. If the infected person defecates outside (near bushes, in a garden, or  field) of if the feces of an infected person are used as fertilizer, eggs are  deposited on soil. They can then mature  and hatch, releasing larvae (immature worms). The larvae mature into a form that can penetrate the skin of humans. Hookworm infection is mainly acquired by walking barefoot on contaminated soil. One kind of hookworm can also be transmitted  through the ingestion of larvae.

    Most people infected  with hookworms have no symptoms. Some  have gastrointestinal symptoms, especially persons who are infected for the  first time. The most serious effects of  hookworm infection are blood loss leading to anemia, in addition to protein loss. Hookworm infections are treatable with  medication prescribed by your health care provider.

     

    FAQS

    What is hookworm?

    Hookworm is an intestinal parasite of humans.  The larvae and adult worms live in the small intestine can cause intestinal disease. The two main species of hookworm infecting  humans are Anclostoma duodenale and Necator americanus.

    How is hookworm spread?

    Hookworm eggs are passed in the feces of an infected  person. If an infected person defecates  outside (near bushes, in a garden, or field) or if the feces from an infected  person are used as fertilizer, eggs are deposited on soil. They can then mature and hatch, releasing  larvae (immature worms). The larvae  mature into a form that can penetrate the skin of humans. Hookworm infection is transmitted primarily  by walking barefoot on contaminated soil. One kind of hookworm (Anclostoma  duodenale)can also be  transmitted through the ingestion of larvae.

    Who is at risk for infection?

    People living in areas with warm and moist climates and where  sanitation and hygiene are poor are at risk for hookworm infection if they walk  barefoot or in other ways allow their skin to have direct contact with contaminated  soil. Soil is contaminated by an infected  person defecating outside or when human feces ("night soil") are used as  fertilizer. Children who play in  contaminated soil may also be at risk.

    What are the signs and symptoms of hookworm?

    Itching and a localized rash are often the first signs of infection. These symptoms occur when the larvae  penetrate the skin. A person with a  light infection may have no symptoms. A  person with a heavy infection may experience abdominal pain, diarrhea, loss of  appetite, weight loss, fatigue and anemia.  The physical and cognitive growth of children  can be affected.

    How is hookworm diagnosed?

    Health care providers can diagnose hookworm by taking a stool sample  and using a microscope to look for the presence of hookworm eggs.

    How can I prevent infection?

    Do not walk barefoot in areas where hookworm is common and where there  may be fecal contamination of the soil. Avoid  other skin-to-soil contact and avoid ingesting such soil. Fecal contamination occurs when people  defecate outdoors or use human feces as fertilizer.  

    The infection of others can be prevented by not defecating outdoors or  using human feces as fertilizer, and by effective sewage disposal systems.

    What is the treatment for hookworm?

    Hookworm infections are generally treated for 1-3 days with medication  prescribed by your health care provider. The drugs are effective and appear to have few side effects. Iron supplements may be prescribed if you  have anemia.

    What is preventive treatment?

    In developing countries, groups at higher risk for soil-transmitted helminth infections (hookworm, Ascaris, and whipworm) are often treated without a prior stool examination. Treating in this way is called preventive treatment (or "preventive chemotherapy"). The high-risk groups identified by the World Health Organization are preschool and school-age children, women of childbearing age (including pregnant women in the 2nd and 3rd trimesters and lactating women) and adults in occupations where there is a high risk of heavy infections. School-age children are often treated through school-health programs and preschool children and pregnant women at visits to health clinics.

    What is mass drug administration (MDA)?

    The soil-transmitted helminths (hookworm, Ascaris, and whipworm) and four other "neglected tropical diseases" (river blindness, lymphatic filariasis, schistosomiasis and trachoma) are sometimes treated through mass drug administrations. Since the drugs used are safe and inexpensive or donated, entire risk groups are offered preventive treatment. Mass drug administrations are conducted periodically (often annually), commonly with drug distributors who go door-to-door. Multiple neglected tropical diseases are often treated simultaneously using MDAs.

     

    EPIDEMIOLOGY & RISK FACTORS

    Hookworm is a soil-transmitted helminth (STH) and is one of the  most common roundworm of humans. Infection is caused by the nematode parasites Necator americanus and Ancylostoma duodenale. Hookworm infections often occur in areas where human feces are used as fertilizer or where defecation onto soil happens.

     

    GEOGRAPHIC DISTRIBUTION

    The geographic distributions of the hookworm species that are  intestinal parasites in human, Ancylostoma  duodenale and Necator americanus, are worldwide in areas with warm, moist climates and are widely  overlapping. Necator americanus was widespread in the Southeastern United States  until the early 20th century.

     

    BIOLOGY

    Causal Agent:

    The human hookworms include the nematode species, Ancylostoma duodenale and Necator americanus.

     

    Life Cycle:

    Life Cycle of Hookworm

    Eggs are passed in the stool, and under favorable conditions (moisture, warmth, shade), larvae hatch in 1 to 2 days. The released rhabditiform larvae grow in the feces and/or the soil, and after 5 to 10 days (and two molts) they become filariform (third-stage) larvae that are infective. These infective larvae can survive 3 to 4 weeks in favorable environmental conditions. On contact with the human host, the larvae penetrate the skin and are carried through the blood vessels to the heart and then to the lungs. They penetrate into the pulmonary alveoli, ascend the bronchial tree to the pharynx, and are swallowed. The larvae reach the small intestine, where they reside and mature into adults. Adult worms live in the lumen of the small intestine, where they attach to the intestinal wall with resultant blood loss by the host. Most adult worms are eliminated in 1 to 2 years, but the longevity may reach several years.

    Some A. duodenale larvae, following penetration of the host skin, can become dormant (in the intestine or muscle). In addition, infection by A. duodenale may probably also occur by the oral and transmammary route. N. americanus, however, requires a transpulmonary migration phase.

    Life cycle image and information courtesy.

     

    DISEASE

    High-intensity hookworm infections occur among both school-age children and adults, soil-transmitted helminthsAscaris and whipworm. High-intensity infections with these worms are  less common among adults. The most  serious effects of hookworm infection are the development of anemia and protein  deficiency caused by blood loss at the site of the intestinal attachment of the  adult worms. When children are  continuously infected by many worms, the loss of iron and protein can retard  growth and mental development.

     

    DIAGNOSIS

    The standard method for diagnosing the presence of hookworm is by identifying  hookworm eggs in a stool sample using a microscope. Because eggs may be difficult to find in  light infections, a concentration procedure is recommended.

     

    PREVENTION AND CONTROL

    The best way to avoid hookworm infection is not to walk barefoot in areas  where hookworm is common and where there may be human fecal contamination of  the soil. Also, avoid other skin contact  with such soil and avoid ingesting it.

    Infection can also be prevented by not defecating outdoors and by effective sewage disposal systems.

    For more information view the source:Center for Disease Control

    <

     

  • ASCARIS LUMBRICOIDES

    An estimated 807-1,221 million people in the world are infected with Ascaris lumbricoides (sometimes called just "Ascaris"). Ascaris, hookworm, and whipworm are known as soil-transmitted helminths (parasitic worms). Together, they account for a major burden of disease worldwide. Ascariasis is now uncommon in the United States.

    Ascaris lives in the intestine and Ascaris eggs are passed in the feces of infected persons. If the infected person defecates outside (near bushes, in a garden, or field) or if the feces of an infected person are used as fertilizer, eggs are deposited on soil. They can then mature into a form that is infective. Ascariasis is caused by ingesting eggs. This can happen when hands or fingers that have contaminated dirt on them are put in the mouth or by consuming vegetables or fruits that have not been carefully cooked, washed or peeled.

    People infected with Ascaris often show no symptoms. If symptoms do occur they can be light and include abdominal discomfort. Heavy infections can cause intestinal blockage and impair growth in children. Other symptoms such as cough are due to migration of the worms through the body. Ascariasis is treatable with medication prescribed by your health care provider.

    FAQS

    What is ascariasis?

    Ascaris is an intestinal parasite of humans. It is the most common human worm infection. The larvae and adult worms live in the small intestine and can cause intestinal disease.

    How is ascariasis spread?

    Ascaris lives in the intestine and Ascaris eggs are passed in the feces of infected persons. If the infected person defecates outside (near bushes, in a garden, or field), or if the feces of an infected person are used as fertilizer, then eggs are deposited on the soil. They can then mature into a form that is infective. Ascariasis is caused by ingesting infective eggs. This can happen when hands or fingers that have contaminated dirt on them are put in the mouth or by consuming vegetables or fruits that have not been carefully cooked, washed or peeled.

    Who is at risk for infection?

    Infection occurs worldwide in warm and humid climates, where sanitation and hygiene are poor, including in temperate zones during warmer months. Persons in these areas are at risk if soil contaminated with human feces enters their mouths or if they eat vegetables or fruit that have not been carefully washed, peeled or cooked. Ascariasis is now uncommon in the United States.

    What are the symptoms of ascariasis?

    People infected with Ascaris often show no symptoms. If symptoms do occur they can be light and include abdominal discomfort. Heavy infections can cause intestinal blockage and impair growth in children. Other symptoms such as cough are due to migration of the worms through the body.

    How is ascariasis diagnosed?

    Health care providers can diagnose ascariasis by taking a stool sample and using a microscope to look for the presence of eggs. Some people notice infection when a worm is passed in their stool or is coughed up. If this happens, bring in the worm specimen to your health care provider for diagnosis.

    How can I prevent infection?

    • Avoid contact with soil that may be contaminated with human feces, including with human fecal matter ("night soil") used to fertilize crops.
    • Wash your hands with soap and warm water before handling food.
    • Teach children the importance of washing hands to prevent infection.
    • Wash, peel, or cook all raw vegetables and fruits before eating, particularly those that have been grown in soil that has been fertilized with manure.

    Transmission of infection to others can be prevented by:

    • not defecating outdoors, and by
    • effective sewage disposal systems.

    What is the treatment for ascariasis?

    Anthelminthic medications (drugs that rid the body of parasitic worms), such as albendazole and mebendazole, are the drugs of choice for treatment. Infections are generally treated for 1-3 days. The recommended medications are effective.

    What is preventive treatment?

    In developing countries, groups at higher risk for soil-transmitted helminth infections (hookworm, Ascaris, and whipworm) are often treated without a prior stool examination. Treating in this way is called preventive treatment (or "preventive chemotherapy"). The high-risk groups identified by the World Health Organization are preschool and school-age children, women of childbearing age (including pregnant women in the 2nd and 3rd trimesters and lactating women) and adults in occupations where there is a high risk of heavy infections. School-age children are often treated through school-health programs and preschool children and pregnant women at visits to health clinics.

    What is mass drug administration (MDA)?

    The soil-transmitted helminths (hookworm, Ascaris, and whipworm) and four other "neglected tropical diseases" (river blindness, lymphatic filariasis, schistosomiasis and trachoma) are sometimes treated through mass drug administrations. Since the drugs used are safe and inexpensive or donated, entire risk groups are offered preventive treatment. Mass drug administrations are conducted periodically (often annually), commonly with drug distributors who go door-to-door. Multiple neglected tropical diseases are often treated simultaneously using MDAs.

    EPIDEMIOLOGY & RISK FACTORS

    Ascaris infection is one of the most common intestinal worm infections. It is found in association with poor personal hygiene, poor sanitation, and in places where human feces are used as fertilizer.

    Geographic Distribution

    The geographic distributions of Ascaris are worldwide in areas with warm, moist climates and are widely overlapping. Infection occurs worldwide and is most common in tropical and subtropical areas where sanitation and hygiene are poor.

    BIOLOGY

    Causal Agent:

    Ascaris lumbricoides is the largest nematode (roundworm) parasitizing the human intestine. (Adult females: 20 to 35 cm; adult male: 15 to 30 cm.)

    Life Cycle:

    Life Cycle of Ascariasis

    Adult worms live in the lumen of the small intestine. A female may produce approximately 200,000 eggs per day, which are passed with the feces. Unfertilized eggs may be ingested but are not infective. Fertile eggs embryonate and become infective after 18 days to several weeks, depending on the environmental conditions (optimum: moist, warm, shaded soil). After infective eggs are swallowed, the larvae hatch, invade the intestinal mucosa, and are carried via the portal, then systemic circulation to the lungs. The larvae mature further in the lungs (10 to 14 days), penetrate the alveolar walls, ascend the bronchial tree to the throat, and are swallowed. Upon reaching the small intestine, they develop into adult worms. Between 2 and 3 months are required from ingestion of the infective eggs to oviposition by the adult female. Adult worms can live 1 to 2 years.

    Life cycle image and information courtesy of DPDx.

    DISEASE

    People infected with Ascaris often show no symptoms. If symptoms do occur they can be light and include abdominal discomfort. Heavy infections can cause intestinal blockage and impair growth in children. Other symptoms such as cough are due to migration of the worms through the body. Ascariasis is treatable with medication prescribed by your health care provider.

    DIAGNOSIS

    The standard method for diagnosing ascariasis is by identifying Ascaris eggs in a stool sample using a microscope. Because eggs may be difficult to find in light infections, a concentration procedure is recommended.

    PREVENTION AND CONTROL

    The best way to prevent ascariasis is to always:

    • Avoid ingesting soil that may be contaminated with human feces, including where human fecal matter ("night soil") or wastewater is used to fertilize crops.
    • Wash your hands with soap and warm water before handling food.
    • Teach children the importance of washing hands to prevent infection.
    • Wash, peel, or cook all raw vegetables and fruits before eating, particularly those that have been grown in soil that has been fertilized with manure.

    For more information view the source:Center for Disease Control

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  • BALANTIDIUM COLI

    Balantidium coli, though rare in the US, is an intestinal protozoan parasite that can infect humans. These parasites can be transmitted through the fecal-oral route by contaminated food and water. Balantidium coli infection is mostly asymptomatic, but people with other serious illnesses can experience persistent diarrhea, abdominal pain, and sometimes a perforated colon. When traveling to  endemic tropical countries, Balantidium coli infection can be prevented by  following good hygiene practices. Wash all fruits and vegetables with clean water when preparing or eating them, even if they have a removable skin.

     

    FAQs

    What is Balantidium coli?

    Balantidium coli is an intestinal protozoan parasite  that causes the infection called balantidiasis. While this type of infection is  less common in the United States, humans and other mammals can become infected with Balantidium coli by ingesting infective cysts from food and water that is contaminated by feces. Mostly asymptomatic, Balantidium infection can cause such symptoms as diarrhea and abdominal pain.

    Where is Balantidium coli endemic?

    Balantidium infection in humans is rare in the United States. However, Balantidium is more common among pigs in warmer climates, and in monkeys in the tropics. Infection in humans is therefore also more common in those areas, especially if good hygiene is not practiced. Balantidium coli is found throughout the world, but it is most prevalent in  tropical and subtropical regions and developing countries.

    How is Balantidium coli transmitted?

    Balantidium coli is transmitted through the  fecal-oral route. Humans can become infected by eating and drinking contaminated  food and water that has come into contact with infective animal or human fecal matter. Infection can occur in several ways, including the following examples:

    • eating  meat, fruits, and vegetables that have been contaminated by an infected person  or contaminated by fecal matter from an infected animal,
    • drinking and washing food  with contaminated water, or
    • having poor hygiene habits.

    What are the signs and symptoms?

    Most people infected with Balantidium coli experience no symptoms. Balantidium coli settles in the large intestine in humans and produces infective microscopic cysts passed in the feces,  potentially leading to more infections or re-infection. People who are  immune-compromised are the most likely to experience more severe signs and symptoms. These include persistent diarrhea, dysentery, abdominal pain, weight loss, nausea, and vomiting. If left untreated, perforation of the colon can occur.

    Is there a test for Balantidium coli infection?

    Yes. Stool samples can be  examined by a lab. Microscopic examination can detect Balantidium coli in the stool.

    Is this  contagious?

    Yes. Balantidium coli is contagious by the fecal-oral route.

    Is there  treatment?

    Yes. The three medications often  used to treat Balantidium coli are tetracycline, metronidazole, and iodoquinol. See your health care  provider for treatment care.

    How can I prevent Balantidium coli?

    Balantidium coli infection can be prevented when traveling to endemic tropical countries by following good hygiene practices. Wash your hands with soap and warm water after using the toilet, changing diapers, and before handling food. Teach children the importance of washing hands to prevent infection. Wash all fruits and vegetables with clean water when preparing or eating them, even if they have a removable skin.

     

    BIOLOGY

    Causal Agent:

    Balantidium coli, a large ciliated protozoan parasite. 

     

    Life Cycle:

     

    Life cycle of Balantidium coli 

    Cysts are the parasite stage responsible for transmission of balantidiasis. The host  most often acquires the cyst through ingestion of contaminated food or water. Following ingestion, excystation occurs in the small intestine, and the trophozoites colonize the large intestine. The trophozoites reside in the lumen of the large intestine of humans  and animals, where they replicate by binary fission, during which  conjugation may occur. Trophozoites undergo encystation to produce infective cysts. Some trophozoites invade the wall of the colon and multiply. Some return to the lumen and disintegrate. Mature cysts are passed with feces.

    Life cycle image and information courtesy of DPDx.

    For more information view the source:Center for Disease Control

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  • BLASTOCYSTIS

    Blastocystis is a genus of single-celled protozoan parasites belonging to a group of organisms known as the Stramenopiles (also called Heterokonts) that includes algae and water molds. Blastocystis comprises several species, living in the gastrointestinal tracts of species as diverse as humans, farm animals, birds, rodents, reptiles, amphibians, fish, and cockroaches.Blastocystis exhibits low host specificity, and many different species of Blastocystis can infect humans and by current convention, any of these species would be identified as Blastocystis hominis if they were identified in a human. These have a widespread geographic distribution and are found at a rate of 5-10% in most developed countries, and a rate of up to 50% in less developed areas. High rates of infection are also found in individuals in developed countries who work with animals. Although the role of Blastocystis hominis in human disease is often referred to as controversial, a systematic survey of research studies conducted by 11 infectious disease specialists from nine countries, found that over 95% of papers published in the last 10 years identified it as causing illness in immunocompetent individuals. The paper attributed confusion over pathogenicity to the existence of asymptomatic carriers, a phenomenon the study noted is common to all gastrointestinal protozoa.

    FAQs

    What is Blastocystis spp.?

    Blastocystis is a common microscopic organism that inhabits the intestine and is found throughout the world. A full understanding of the biology of Blastocystis and its relationship to other organisms is not clear, but is an active area of research. Infection with Blastocystis is called blastocystosis.

    What are the symptoms of infection with Blastocystis?

    Watery or loose stools, diarrhea, abdominal pain, anal itching, weight loss, constipation, and excess gas have all been reported in persons with Blastocystis infection. Many people have no symptoms at all. The organism can be found in both well and sick persons.

    How long will I be infected?

    Blastocystis can remain in the intestine for weeks, months, or years.

    Is Blastocystis spp. the cause of my symptoms?

    The role of Blastocystis in causing disease is controversial among experts. Some types of Blastocystis may be more likely to be associated with symptoms. Finding Blastocystis in stool samples should be followed up with a careful search for other possible causes of your symptoms.

    Is having blastocystosis common?

    Yes. In fact, many people have Blastocystis in their intestine, some without ever having symptoms.

    What should I do if I think I have blastocystosis?

    See your health care provider who will ask you to provide stool samples for testing. Diagnosis may be difficult, so you may be asked to submit several stool samples.

    Is medication available to treat blastocystosis?

    Yes. Drugs are available by prescription to treat blastocystosis. However, sometimes medication is not effective, and a search for other possible causes of your symptoms may be necessary.

    How did I get blastocystosis?

    How Blastocystis is transmitted is not known for certain, although the number of people infected seems to increase in areas where sanitation and personal hygiene is not adequate. Studies have suggested that risk of infection may increase through: ingesting contaminated food or water, exposure to a day care environment, or exposure to animals.

    How can I prevent infection with Blastocystis?

    Wash your hands with soap and warm water after using the toilet, changing diapers, and before handling food. Teach children the importance of washing hands to prevent infection. Avoid water or food that may be contaminated. Wash and peel all raw vegetables and fruits before eating. When traveling in countries where the water supply may be unsafe, avoid drinking unboiled tap water and avoid uncooked foods washed with unboiled tap water. Bottled or canned carbonated beverages, seltzers, pasteurized fruit drinks, and steaming hot coffee and tea are safe to drink.

    Should I be concerned about spreading infection to the rest of my household?

    There is little risk of spreading infection if you practice adequate personal hygiene. This includes thorough hand washing with soap and warm water after using the toilet and before handling food.

    BIOLOGY

    Causal Agent

    The taxonomic classification of Blastocystis hominis is mired in controversy. It has been previously considered as yeasts, fungi, or ameboid, flagellated, or sporozoan protozoa. Recently, however, based on molecular studies, especially dealing with the sequence information on the complete SSUrRNA gene, B. hominis has been placed within an informal group, the stramenopiles (Silberman et al. 1996). Stramenopiles are defined, based on molecular phylogenies, as a heterogeneous evolutionary assemblage of unicellular and multicellular protists including brown algae, diatoms, chrysophytes, water molds, slime nets, etc. (Patterson, 1994). Cavalier-Smith (1998) considers stramenopiles to be identical to his infrakingdom Heterokonta under the kingdom Chromista. Therefore, according to Cavalier-Smith, B. hominis is a heterokontid chromista.

    Life Cycle:

    Proposed life cycle of blastocystis hominis

    Knowledge of the life cycle and transmission is still under investigation, therefore this is a proposed life cycle for B. hominis. The classic form found in human stools is the cyst, which varies tremendously in size from 6 to 40 µm. The thick-walled cyst present in the stools is believed to be responsible for external transmission, possibly by the fecal-oral route through ingestion of contaminated water or food . The cysts infect epithelial cells of the digestive tract and multiply asexually. Vacuolar forms of the parasite give origin to multi vacuolar and ameboid forms. The multi-vacuolar develops into a pre-cyst that gives origin to a thin-walled cyst, thought to be responsible for autoinfection. The ameboid form gives origin to a pre-cyst, which develops into thick-walled cyst by schizogony. The thick-walled cyst is excreted in feces.

    Life cycle image and information courtesy of DPDx.

    For more information view the source:Center for Disease Control


    << Back to Wiki

  • BLASTOCYSTIS HOMINIS

    Blastocystis is a genus of single-celled protozoan parasites belonging to a group of organisms known as the Stramenopiles (also called Heterokonts) that includes algae and water molds. Blastocystis comprises several species, living in the gastrointestinal tracts of species as diverse as humans, farm animals, birds, rodents, reptiles, amphibians, fish, and cockroaches.Blastocystis exhibits low host specificity, and many different species of Blastocystis can infect humans and by current convention, any of these species would be identified as Blastocystis hominis if they were identified in a human. These have a widespread geographic distribution and are found at a rate of 5-10% in most developed countries, and a rate of up to 50% in less developed areas. High rates of infection are also found in individuals in developed countries who work with animals. Although the role of Blastocystis hominis in human disease is often referred to as controversial, a systematic survey of research studies conducted by 11 infectious disease specialists from nine countries, found that over 95% of papers published in the last 10 years identified it as causing illness in immunocompetent individuals. The paper attributed confusion over pathogenicity to the existence of asymptomatic carriers, a phenomenon the study noted is common to all gastrointestinal protozoa.

    FAQs

    What is Blastocystis spp.?

    Blastocystis is a common  microscopic organism that inhabits the intestine and is found  throughout the world. A full  understanding of the biology of Blastocystis and its relationship to other organisms is not clear, but is an active area of  research. Infection with Blastocystis is  called blastocystosis.

    What are the symptoms of infection with Blastocystis?

    Watery  or loose stools, diarrhea, abdominal pain, anal itching, weight loss, constipation,  and excess gas have all been reported in persons with Blastocystis infection. Many people have no symptoms at all. The organism can be found in both well and sick persons.

    How long will I be infected?

    Blastocystis can remain in the  intestine for weeks, months, or years.

    Is Blastocystis spp. the cause of my symptoms?

    The  role of Blastocystis in causing  disease is controversial among experts. Some  types of Blastocystis may be more  likely to be associated with symptoms. Finding Blastocystis in stool samples should be followed up  with a careful search for other possible causes of your symptoms.

    Is having blastocystosis common?

    Yes. In fact, many people have Blastocystis in their intestine, some without ever having symptoms.

    What should I do if I think I have blastocystosis?

    See  your health care provider who will ask you to provide stool samples for  testing. Diagnosis may be difficult, so you may be asked to submit several  stool samples.

    Is medication available to treat blastocystosis?

    Yes. Drugs are available by prescription to treat blastocystosis. However, sometimes  medication is not effective, and a search for other possible causes of your  symptoms may be necessary.

    How did I get blastocystosis?

    How Blastocystis is transmitted is not known for  certain, although the number of people infected seems to increase in areas  where sanitation and personal hygiene is not adequate. Studies have suggested that risk of infection may increase through: ingesting contaminated food or water,    exposure to a day care environment, or   exposure to animals.

    How can I prevent infection with Blastocystis?

    Wash your hands with soap and warm water after using the toilet, changing diapers, and before handling food. Teach children the importance of washing hands to prevent infection.       Avoid water or food that may be contaminated.     Wash and peel all raw vegetables and fruits before eating.     When traveling in countries where the water supply may be unsafe, avoid drinking unboiled tap water and avoid uncooked foods washed with unboiled tap water. Bottled or canned carbonated beverages, seltzers, pasteurized fruit drinks, and steaming hot coffee and tea are safe to drink.

    Should I be concerned about spreading infection to the rest of my household?

    There is  little risk of spreading infection if you practice adequate personal hygiene. This includes thorough hand washing with soap and warm water after using the toilet and before handling food.

    BIOLOGY

    Causal Agent

    The taxonomic   classification of Blastocystis hominis is mired in controversy. It has been previously considered as yeasts, fungi, or ameboid, flagellated, or   sporozoan protozoa. Recently, however, based on molecular studies, especially   dealing with the sequence information on the complete SSUrRNA gene, B. hominis has been placed within an informal group, the stramenopiles   (Silberman et al. 1996). Stramenopiles are defined, based on molecular   phylogenies, as a heterogeneous evolutionary assemblage of unicellular and   multicellular protists including brown algae, diatoms, chrysophytes, water   molds, slime nets, etc. (Patterson, 1994). Cavalier-Smith (1998) considers   stramenopiles to be identical to his infrakingdom Heterokonta under the kingdom   Chromista. Therefore, according to Cavalier-Smith, B. hominis is a   heterokontid chromista.

    Life Cycle:

    Proposed life cycle of blastocystis hominis

    Knowledge of the life   cycle and transmission is still under investigation, therefore this is a   proposed life cycle for B. hominis. The classic form found in human   stools is the cyst, which varies tremendously in size from 6 to 40 µm. The thick-walled cyst present in the stools is believed to be responsible for external transmission,   possibly by the fecal-oral route through ingestion of contaminated water or food . The cysts infect epithelial cells of the digestive tract and  multiply asexually. Vacuolar forms of the parasite give origin to multi vacuolar and ameboid forms. The multi-vacuolar develops into a pre-cyst that gives origin to a thin-walled cyst, thought to be responsible for autoinfection. The ameboid   form gives origin to a pre-cyst, which develops into thick-walled cyst by schizogony. The thick-walled cyst is excreted in feces.

    Life cycle image and information courtesy of DPDx.

    For more information view the source:Center for Disease Control

    <

  • CLONORCHIS

    Clonorchis sinensis, the Chinese liver fluke, is a human liver fluke in the class Trematoda, Phylum Platyhelminthes. This parasite lives in the liver of humans, and is found mainly in the common bile duct and gall bladder, feeding on bile. These animals, which are believed to be the third most prevalent worm parasite in the world, are endemic to Japan, China, Taiwan, and Southeast Asia, currently infecting an estimated 30,000,000 humans. The egg of a Clonorchis sinensis (commonly: human liver fluke), which contains the miracidium that develops into the adult form, floats in freshwater until it is eaten by a snail. First intermediate host. Freshwater snail Parafossarulus manchouricus - synonym: Parafossarulus striatulus, often serves as a first intermediate host for Clonorchis sinensis in China, Japan, Korea and Russia. Other snail hosts include: Bithynia longicornis - synonym: Alocinma longicornis - in China Bithynia fuchsiana - in China Bithynia misella - in China Parafossarulus anomalosiralis - in China Melanoides tuberculata - in China Semisulcospira libertina - in China Assiminea lutea - in China Tarebia granifera - in Taiwan, China Once inside of the snail body, the miracidium hatches from the egg, and parasitically grows inside of the snail. The miracidium develops into a sporocyst, which in turn house the asexual reproduction of redia, the next stage. The redia themselves house the asexual reproduction of free-swimming cercaria. This system of asexual reproduction allows for an exponential multiplication of cercaria individuals from one miracidium. This aids the Clonorchis in reproduction, because it enables the miracidium to capitalize on one chance occasion of passively being eaten by a snail before the egg dies. Once the redia mature, having grown inside the snail body until this point, they actively bore out of the snail body into the freshwater environment. Second intermediate hostThere, instead of waiting to be consumed by a host (as is the case in their egg stage), they seek out a fish. Boring their way into the fish's body, they again become parasites of their new hosts. Once inside of the fish muscle, the cercaria create a protective metacercarial cyst with which to encapsulate their bodies. This protective cyst proves useful when the fish muscle is consumed by a human. Definitive hostThe acid-resistant cyst enables the metacercaria to avoid being digested by the human gastric acids, and allows the metacercaria to reach the small intestine unharmed. Reaching the small intestines, the metacercaria navigate toward the human liver, which becomes its final habitat. Clonorchis feed on human bile created by the liver. In the human liver, the mature Clonorchis reaches its stage of sexual reproduction. The hermaphroditic adults produce eggs every 1?30 seconds, resulting in the rapid multiplication of inhabitants in the liver. This leads to various health problems.

     

    EFFECTS ON HUMAN HEALTH

    Dwelling in the bile ducts, Clonorchis induces an inflammatory reaction, epithelial hyperplasia and sometimes even cholangiocarcinoma, the incidence of which is raised in fluke-infested areas. One adverse effect of Clonorchis is the possibility for the adult metacercaria to consume all bile created in the liver, which would inhibit the host human from digesting, especially fats. Another possibility is obstruction of the bile duct by the parasite or its eggs, leading to biliary obstruction and cholangitis (specifically oriental cholangitis). Central Serous Retinopathy (CSR) a report of 80 cases by Dr. John Chiao-nan Chang, M.D. and Dr. Yin-Ping Wang, M.D. Hong Kong on page 125 of their report observed that 19% of the cases of CSR in their sample tested positive for Clonorchis sinensis.

    SYMPTOMS

    Dwelling in the bile ducts, Clonorchis induces an inflammatory reaction, epithelial hyperplasia and sometimes even cholangiocarcinoma, the incidence of which is raised in fluke-infested areas.  One adverse effect of Clonorchis is the possibility for the adult metacercaria to consume all bile created in the liver, which would inhibit the host human from digesting, especially fats. Another possibility is obstruction of the bile duct by the parasite or its eggs, leading to biliary obstruction and cholangitis (specifically oriental cholangitis).  Central Serous Retinopathy (CSR) a report of 80 cases by Dr. John Chiao-nan Chang, M.D. and Dr. Yin-Ping Wang, M.D. Hong Kong on page 125 of their report observed that 19% of the cases of CSR in their sample tested positive for Clonorchis sinensis.

    DIAGNOSIS AND TREATMENT

    Post infectious microscopic demonstration in stools or in duodenal aspirate is the most practical diagnostic method. Morphological comparison with other GI parasites is performed. Drugs used to treat infestation include triclabendazole, praziquantel, bithionol, albendazole and mebendazole.

     

    LIFE CYCLE

     

    Life cycle of Clonorchis sinensis

    For more information view the source:Wikipedia

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  • CRYPTOSPORIDIUM PARVUM

    Cryptosporidium is a microscopic parasite that causes the diarrheal disease cryptosporidiosis. Both the parasite and the disease are commonly known as "Crypto."

    There are many species of Cryptosporidium that infect humans and animals. The parasite is protected by an outer  shell that allows it to survive outside the body for long periods of  time and makes it very tolerant to chlorine disinfection.

    While this parasite can be spread in several different ways, water (drinking water and recreational water) is the most common method of transmission. Cryptosporidium is one of the most frequent causes of waterborne disease among humans in the United States.

    EPIDEMIOLOGY & RISK FACTORS

    Crypto lives in the intestine of infected humans or animals. An infected person or animal sheds Cryptosporidium parasites in the stool. Millions of Crypto parasites can be released in  a bowel movement from an infected human or animal. Shedding begins when  the symptoms begin and can last for weeks after the symptoms (e.g.,  diarrhea) stop. You can become infected after accidentally swallowing  the parasite. Crypto may be found in soil, food, water, or surfaces  that have been contaminated with the feces from infected humans or  animals. Crypto is not spread by contact with blood. Crypto can be  spread:

    • By putting something in your mouth or  accidentally swallowing something that has come in contact with the  stool of a person or animal infected with Crypto.

    Recreational water can be contaminated with sewage or feces from humans or animals.    

    • By swallowing water or beverages contaminated by stool from infected humans or animals.
    • By  eating uncooked food contaminated with Crypto. All fruits and  vegetables you plan to eat raw should be thoroughly washed with  uncontaminated water.
    • By touching your mouth with contaminated hands. Hands can become contaminated through a variety of activities, such as:            
    • touching  surfaces (e.g., toys, bathroom fixtures, changing tables, diaper pails)  that have been contaminated by stool from an infected person,
    • changing diapers,
    • caring for an infected person, and
    • handling an infected cow or calf.
    • People with greater exposure to contaminated materials are more at risk for infection, such as:    
    • Children who attend day care centers, including diaper-aged children
    • Child care workers
    • Parents of infected children
    • People who take care of other people with cryptosporidiosis
    • International travelers
    • Backpackers, hikers, and campers who drink unfiltered, untreated water
    • People who drink from untreated shallow, unprotected wells
    • People, including swimmers, who swallow water from contaminated sources
    • People who handle infected cattle
    • People exposed to human feces through sexual contact

    Contaminated water may include water that has not been boiled or filtered, as well as contaminated recreational water sources. Several community-wide outbreaks of cryptosporidiosis have  been linked to drinking municipal water or recreational water  contaminated with Cryptosporidium.

    Cryptosporidium parasites are found in every region of the United States and throughout  the world. Travelers to developing countries may be at greater risk for  infection because of poorer water treatment and food sanitation, but  cryptosporidiosis occurs worldwide. In the United States, an estimated 748,000 cases of cryptosporidiosis occur each year.

    Once  infected, people with decreased immunity are most at risk for severe  disease. The risk of developing severe disease may differ depending on  each person's degree of immune suppression.

    BIOLOGY

    Causal Agent:

    Many species of Cryptosporidium exist that infect humans and a wide range of animals. Although Cryptosporidium parvum and Cryptosporidium hominis (formerly known as C. parvum anthroponotic genotype or genotype 1) are the most prevalent species causing disease in humans, infections by C. felis, C. meleagridis, C. canis, and C. muris have also been reported.

    Life Cycle:

    Sporulated oocysts, containing 4 sporozoites, are excreted by the infected host through feces and possibly other routes such as respiratory secretions. Transmission of Cryptosporidium parvum and C. hominis occurs mainly through contact with contaminated water (e.g., drinking or recreational water). Occasionally food sources, such as chicken salad, may serve as vehicles for transmission. Many outbreaks in the United States have occurred in waterparks, community swimming pools, and day care centers. Zoonotic and anthroponotic transmission of C. parvum and anthroponotic transmission of C. hominisoccur through exposure to infected animals or exposure to water contaminated by feces of infected animals. Following ingestion (and possibly inhalation) by a suitable host, excystation occurs. The sporozoites are released and parasitize epithelial cells of the gastrointestinal tract or other tissues such as the respiratory tract. In these cells, the parasites undergo asexual multiplication (schizogony or merogony) and then sexual multiplication (gametogony) producing microgamonts (male) and macrogamonts (female). Upon fertilization of the macrogamonts by the microgametes, oocystdevelop that sporulate in the infected host. Two different types of oocysts are produced, the thick-walled, which is commonly excreted from the host, and the thin-walled oocyst, which is primarily involved in autoinfection. Oocysts are infective upon excretion, thus permitting direct and immediate fecal-oral transmission.

    Life cycle image and information courtesy of DPDx.

    DISEASE

    Symptoms of cryptosporidiosis generally begin 2 to 10 days (average  7 days) after becoming infected with the parasite. The most common  symptom of cryptosporidiosis is watery diarrhea. Other symptoms include:

     

    • Stomach cramps or pain
    • Dehydration
    • Nausea
    • Vomiting
    • Fever
    • Weight loss

    Some people with Crypto will have no symptoms at all.

    Symptoms  usually last about 1 to 2 weeks (with a range of a few days to 4 or  more weeks) in persons with healthy immune systems. Occasionally,  people may experience a recurrence of symptoms after a brief period of  recovery before the illness ends. Symptoms can come and go for up to 30  days.  While the small intestine is the site most commonly affected, Cryptosporidium infections could possibly affect other areas of the digestive tract or the respiratory tract. People  with weakened immune systems may develop serious, chronic, and  sometimes fatal illness. Examples of people with weakened immune  systems include:

    • people with AIDS;
    • those with inherited diseases that affect the immune system; and
    • cancer and transplant patients who are taking certain immunosuppressive drugs.

    The risk of developing severe disease may differ depending on each person's degree of immune suppression.

    DIAGNOSIS

    Diagnosis of cryptosporidiosis is made by examination of stool samples. Because detection of Cryptosporidium can be difficult, patients may be asked to submit several stool samples  over several days. Most often, stool specimens are examined  microscopically using different techniques (e.g., acid-fast staining,  direct fluorescent antibody [DFA] , and/or enzyme immunoassays for  detection of Cryptosporidium sp. antigens).

    Molecular  methods (e.g., polymerase chain reaction – PCR) are increasingly used  in reference diagnostic labs, since they can be used to identify Cryptosporidium spp. at the species level.  Tests for Cryptosporidium are not routinely done in most laboratories; therefore, health care  providers should specifically request testing for this parasite.

    PREVENTION AND CONTROL

    • Practice good hygiene
    • Wash hands with soap and water for at least 20 seconds, rubbing hands together vigorously and scrubbing all surfaces:             
    • Before preparing or eating food
    • After using the toilet
    • After changing diapers or cleaning up a child who has used the toilet
    • Before and after tending to someone who is ill with diarrhea
    • After handling an animal or animal waste
    • At child care facilities
    • To reduce the risk of disease transmission, children with diarrhea should be excluded from child care settings until the diarrhea has stopped.
    • At recreational water venues (pools, interactive fountains, lakes, ocean)
    • Protect others by not swimming if you are experiencing diarrhea (this is essential for children in diapers). If diagnosed with cryptosporidiosis, do not swim for at least 2 weeks after diarrhea stops.
    • Shower before entering the water.
    • Wash children thoroughly (especially their bottoms) with soap and water after they use the toilet or their diapers are changed and before they enter the water.
    • Take children on frequent bathroom breaks and check their diapers often.
    • Change diapers in the bathroom, not at the poolside.
    • Around animals
    • Minimize contact with the feces of all animals, particularly young animals.
    • When cleaning up animal feces, wear disposable gloves, and always wash hands when finished.
    • Wash hands after any contact with animals or their living areas.
    • Wash hands after gardening, even if wearing gloves.
    • Immunocompromised persons
    • Avoid close contact with any person or animal that has cryptosporidiosis. Cryptosporidiosis can become a life threatening disease for immunocompromised persons.
    • Do not handle animal feces because infection can be life threatening for immunocompromised persons.
    • Avoid Water That Might Be Contaminated
    • You may not be protected in a chlorinated recreational water venue  (for example, swimming pool, water park, water play area, splash pad, spray pad) because Cryptosporidium is chlorine-resistant and can live for days in chlorine-treated water.
    • Do not swallow water while swimming in swimming pools, hot tubs, interactive fountains, lakes, rivers, springs, ponds, streams or the ocean.
    • Reduce  contamination of treated recreational water venues by having pool operators install in-line secondary disinfection systems (for example, ultraviolet light, ozone) to inactive this chlorine-tolerant parasite.
    • Do not drink untreated water from lakes, rivers, springs, ponds, streams, or shallow wells.
    • Do not drink inadequately treated water or ice made from water during communitywide outbreaks caused by contaminated drinking water.
    • Do not use or drink inadequately treated water or use ice when traveling in countries where the water supply might be unsafe.
    • If the safety of drinking water is questionable (for example, outbreak, poor sanitation, lack of water treatment systems):             
    • Drink bottled water
    • Disinfect it by heating the water to a rolling boil for 1 minute, or
    • Use a filter that has been tested and rated by National Safety Foundation (NSF) Standard 53 or NSF Standard 58 for cyst and oocyst reduction; filtered water will need additional treatment to kill or inactivate bacteria and viruses

    For more information view the source:Center for Disease Control

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  • DIENTAMOEBA FRAGILIS

    DIENTAMOEBA FRAGILIS

    Dientamoeba fragilis is a parasite that causes gastrointestinal problems. Despite its name, Dientamoeba fragilis is not an ameba but a flagellate. This protozoan parasite produces trophozoites; cysts have not been identified. Infection may be either symptomatic or asymptomatic.

    FAQs

    What is Dientamoeba fragilis?

    Dientamoeba fragilis is a parasite that lives in the large intestine of humans. Infection is common worldwide, including in the United States.

    What are the symptoms of infection with Dientamoeba fragilis?

    Many infected people do not have any symptoms. The most common symptoms are diarrhea and abdominal pain. Loss of appetite and weight loss, nausea, and fatigue also are common. The infection does not spread from the intestine to other parts of the body.

    What should I do if I think I might be infected?

    See your health care provider.

    How is infection with Dientamoeba fragilis diagnosed?

    Your health care provider will ask you to provide stool samples for testing. Because the parasite is not always found in every stool sample, you might be asked to submit stool samples from more than one day. You might also be tested for pinworm eggs, which are commonly (but not always) found in persons infected with D. fragilis.

    Is medication available to treat infection with Dientamoeba fragilis?

    Yes. Safe and effective medications are available for D. fragilis infections.

    How did I get infected with Dientamoeba fragilis?

    This question is difficult to answer because we aren't sure how D. fragilis is spread. The parasite is fragile and probably cannot live very long in the environment. Infection might be spread by:

    • Accidentally swallowing pinworm eggs (which might protect this fragile parasite) or the eggs of another parasite.
    • Swallowing something, such as food or water, or touching to your mouth something contaminated with stool from someone infected with D. fragilis.

    Who is at greatest risk for infection?

    Anyone can become infected with this parasite. However, the risk for infection might be higher for people who have weak immune systems and those who live in or travel to settings with poor sanitary conditions.

    How can I prevent Dientamoeba fragilis infection?

    • Wash your hands with soap and warm water after using the toilet, changing diapers, and before preparing foods.
    • Teach children the importance of washing hands to prevent infection.

     

    BIOLOGY

    Causal Agent:

    Despite its name, Dientamoeba fragilis is not an ameba but a flagellate. This protozoan parasite produces trophozoites; cysts have not been identified. Infection may be either   symptomatic or asymptomatic.

     

    Life Cycle

    Life

    The complete life cycle of this parasite has not yet been determined, but assumptions were made based on clinical data. To date, the cyst stage has not been identified in D. fragilis life cycle, and the trophozoite is the only stage found in stools of infected individuals. D. fragilis is probably transmitted by fecal-oral route.The and transmission via helminth eggs (e.g., Ascaris, Entamoeba spp has been postulated. Trophozoites of D. fragilis have characteristically one or  two nuclei and it is found in children complaining of intestinal (e.g.,   intermittent diarrhea, abdominal pain) and other symptoms (e.g., nausea,   anorexia, fatigue, malaise, poor weight gain).

    Life cycle image and information courtesy of DPDx.

    For more information view the source:Center for Disease Control

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  • DIPYLIDIUM CANINUM

    Dipylidium caninum, also called the cucumber tapeworm or the double-pore tapeworm, is a cyclophyllid cestode that infects organisms afflicted with fleas, including canids, felids, and pet-owners, especially children. Adult worms are about 18 inches long. Eggs (or “egg clusters” or “egg balls”) are passed in the host's feces and ingested by fleas, which are in turn ingested by another mammal after the tapeworm larvae partially develop. Examples of fleas that can spread D. caninum include: Ctenocephalides canis and Ctenocephalides felis.

    As in all members of family Dipylidiidae, proglottids of the adult have genital pores on both sides (hence the name double-pore tapeworm). Each side has a set of male and female reproductive organs. The scolex has a rostellum with four rows of hooks, along with the four suckers that all cyclophyllid cestodes have. In cats, sometimes proglottids are visible hanging out of a cat's anus.

    Inside fleas, eggs hatch and form oncosphere larvae that move through the wall of the flea intestine into the body cavity where they become cysticercoid larvae, which are infective to mammal hosts.

    In children, infection causes diarrhea and restlessness. As with most tapeworm infections, the drugs of choice are niclosamide or praziquantel. The best way to prevent human infection is to treat infected animals and to kill fleas.

    Although, D. Caninum is usually transferred via a flea, Trichodectes canis, the chewing louse of dogs, can also be the intermediate host for the tapeworm.

     

    FAQs

    What is the most common kind of tapeworm dogs and cats get?

    The most  common tapeworm of dogs and cats in the United States is called Dipylidium caninum.  Infection is common and found throughout the world.

     

    How did my pet get the Dipylidium tapeworm?

    By swallowing a flea infected with a tapeworm larvae. A dog or cat may swallow a flea while self-grooming. Once the flea is digested by the dog or cat, the larval  tapeworm is able to develop into an adult tapeworm.

    The adult tapeworm is made up of many small segments, called proglottids, each about the size of a grain of rice. Adult tapeworms may measure 4-28 inches in length. As the tapeworm matures inside the intestine, these segments (proglottids) break off and pass into the stool.

     

    How would I know if my pet has a tapeworm infection?

    Although cats and  dogs are rarely ill as a result of a Dipylidium tapeworm  infection, the proglottids can sometimes be seen crawling near the anus or on  the surface of a fresh bowel movement. Proglottids contain tapeworm eggs; these  eggs are released into the environment when the proglottid dries out. The dried  proglottids are small (about 2 mm), hard and yellowish in color and can  sometimes be seen stuck to the fur around the pet's anus.

     

    What kind of problems do tapeworms cause for the dog?

    Tapeworms are not  usually harmful to your pet. Weight loss may occur if your pet is heavily  infected. Sometimes, an infected dog will & quot; scoot & quot; or drag its anus  across the ground or carpet because the segments are irritating to the skin in  this area.

    Occasionally, a  portion of this tapeworm will be passed when the dog vomits. If this happens, a  worm several inches long may be seen.

     

    How is tapeworm infection diagnosed in my pet?

    Tapeworm infection  is usually diagnosed when the moving segments are seen crawling around the anus  or in a bowel movement. Dipylidium tapeworm eggs are  rarely released into the feces and are therefore not usually detected by  routine fecal exams performed by your veterinarian. Because of this,  veterinarians depend on you to notify them of possible tapeworm infection in  your pet.

     

    Can I get a tapeworm infection from my pet?

    Yes; however, the risk of infection with this  tapeworm in humans is very low. For a person to become infected with Dipylidium, he or she must  accidentally swallow an infected flea. Most reported cases involve children.  The most effective way to prevent infections in pets and humans is through flea  control. A child who is infected will usually pass proglottids (or what appears  as rice) in a bowel movement or find them stuck to the skin around the anal  area.

     

    How is tapeworm infection treated?

    Treatment for both animals and humans is simple and very effective. A prescription drug called praziquantel is given, either orally or by injection (pets only). The medication causes the tapeworm to dissolve within the intestine. Since the worm is usually digested before it passes, it may not be visible in your dog's stool. The drugs are generally well-tolerated.

     

    What should I do if I think my child is infected with tapeworms?

    See your health care provider for diagnosis and treatment.

     

    How can tapeworm infection be prevented?

    To reduce the likelihood of infection you should:

    • Control fleas on your pet, and in their indoor and outdoor environments.
    • Have your veterinarian treat your dogs and cats promptly if they have tapeworms.
    • Clean up after your pet, especially in playgrounds and public parks. Bury the feces, or place it in a plastic bag and dispose of it in the trash.
    • Do not allow children to play in areas that are soiled with pet or other animal feces.
    • Teach children to always wash their hands after playing with dogs and cats, and after playing outdoors.

     

    BIOLOGY

    Causal Agent:

    Dipylidium caninum (the double-pored dog tapeworm) mainly infects dogs and cats, but is occasionally found in humans.

     

    Life Cycle:

    Proposed life cycle of blastocystis hominis

    Gravid proglottids are   passed intact in the feces or emerge from the perianal region of the host. Subsequently they release typical egg packets. On rare occasions, proglottids rupture and egg packets are seen in   stool samples. Following ingestion of an egg by the intermediate host (larval   stages of the dog or cat flea Ctenocephalides spp.), an oncosphere is   released into the flea's intestine. The oncosphere penetrates the intestinal   wall, invades the insect's hemocoel (body cavity), and develops into a   cysticercoid larva. The larva develops into an adult, and the adult flea harbours the   infective cysticercoid. The vertebrate host becomes infected by ingesting the adult flea   containing the cysticercoid. The dog is the principal definitive host for Dipylidium   caninum. Other potential hosts include cats, foxes, and humans (mostly   children). Humans acquire infection by ingesting the cysticercoid contaminated   flea. This can be promulgated by close contact between children and their   infected pets. In the small intestine of the vertebrate host the cysticercoid   develops into the adult tapeworm which reaches maturity about 1 month after   infection. The adult tapeworms (measuring up to 60 cm in length and 3   mm in width) reside in the small intestine of the host, where they each attach   by their scolex. They produce proglottids (or segments) which have two genital   pores (hence the name "double-pored" tapeworm). The proglottids mature, become   gravid, detach from the tapeworm, and migrate to the anus or are passed in the   stool.

    Life cycle image and information courtesy of DPDx.

    For more information view the source:Center for Disease Control

     

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  • ENDOLIMAX NANA

    Although much literature cites this parasite as a non-pathogen, there is much reason to believe that in some cases these "non-pathogenic" agents actually cause symptoms in patients, with no other infections or conditions that would explain their symptoms. Following is a list of a few references to support that statement: Cuffari C, Oligny L, Siedman EG, 1998 Dientamoeba fragilis masquerading as allergic colitis. J. Pediatr Gastroenterol Nutr 26: 16-20., Feigin, RD, Cherry, James, Demmler-Harrison, GJ, and Kaplan, SL. Feigin and Cherry's Textbook of Pediatric Infectious Diseases, 6th Edition; Ch. 223, Amin, OM, 2002. Seasonal Prevalence of Intestinal Parasites in the United States During 2000. Am J. Trop. Med. Hyg., 66(6), 799-803., Garcia LS, 2005. Diagnostic Medical Parasitology. Washington, DC: American Society for Microbiology. Pg. 9 

     

    BIOLOGY

    CAUSAL AGENTS

    Entamoeba coli, E. hartmanni, E. polecki, Endolimax nana, and Iodamoeba buetschlii are generally considered nonpathogenic and reside in the large intestine of the human host. Entamoeba gingivalis is also considered nonpathogenic and resides in the oral cavity of the human host, in the gingival pockets at the base of the teeth.

     

    LIFE CYCLE

    Entamoeba coli, E. hartmanni, E. polecki, Endolimax nana, and Iodamoeba buetschlii are generally considered nonpathogenic and reside in the large intestine of the human host . Both cysts and trophozoites of these species are passed in stool and considered diagnostic . Cysts are typically found in formed stool, whereas trophozoites are typically found in diarrheal stool. Colonization of the nonpathogenic amebae occurs after ingestion of mature cysts in fecally-contaminated food, water, or fomites . Excystation occurs in the small intestine and trophozoites are released, which migrate to the large intestine. The trophozoites multiply by binary fission and produce cysts, and both stages are passed in the feces . Because of the protection conferred by their cell walls, the cysts can survive days to weeks in the external environment and are responsible for transmission. Trophozoites passed in the stool are rapidly destroyed once outside the body, and if ingested would not survive exposure to the gastric environment.

     

    LIFE CYCLE (Entamoeba gingivalis):

    There is no known cyst stage for Entamoeba gingivalis; trophozoites live in the oral cavity of humans, residing in the gingival pockets near the base of the teeth . They are not considered pathogenic, and feed on bacteria and other debris. Trophozoites are transmitted person-to-person orally by kissing or fomites (such as eating utensils) . The trophozoite stage of E. gingivalis is morphologically similar to that of E. histolytica, and the two should be differentiated, as both can be coughed up in sputum specimens (for the latter, when present in pulmonary abscesses).

     

    GEOGRAPHIC DISTRIBUTION

    All six species are distributed worldwide. Entamoeba polecki in nature is primarily a parasite of pigs and monkeys, and human infection is more prevalent in areas where the people have animal contact.

     

    CLINICAL FEATURES

    Entamoeba coli, E. hartmanni, E. polecki, Endolimax nana, and Iodamoeba buetschlii are generally considered nonpathogenic, although they have been found in the stool of patients presenting with diarrhea where no known pathogens were identified. Their presence in stool can be an indicator of fecal contamination of a food or water source, and does not rule-out the presence of other parasites. Entamoeba gingivalis is also considered nonpathogenic, but is found in about 95% of patients with gum disease and about 50% of patients with healthy gums.

     

    LABORATORY DIAGNOSIS

    For E. coli, E. hartmanni, E. polecki, E. nana, and I. buetschlii, identification is made by observing cysts and/or trophozoites in stool specimens, both concentrated wet mounts and permanent stained smears. Identification of E. gingivalis is made by the finding of trophozoites in scrapings of the gums and teeth. They may also be found in sputum in rare occasions. As such, it is important to differentiate them from the morphologically-similar trophozoites of E. histolytica, which may be found in sputum from pulmonary abscesses.

    For more information view the source:Center for Disease Control

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  • ENDOLIMAX NANA CYSTS

    Endolimax is a genus of amoebozoa that are found in the intestines of various animals, including the species E. nana found in humans. Originally thought to be non-pathogenic, studies suggest it can cause intermittent or chronic diarrhea. Additionally, it is very significant in medicine because it can provide false positives for other tests, notably the similar species Entamoeba histolytica, the pathogen responsible for amoebic dysentery, and because its presence indicates the host has consumed fecal material. It forms cysts with four nuclei which excyst in the body and become trophozoites. Endolimax nana nuclei have a large endosome somewhat off-center and small amounts of visible chromatin or none at all.

    CYSTS

    Cysts are small, with a spherical to ellipsoidal shape. Mature cysts contain four nuclei; immature cysts are rarely seen. These cysts measure 5-10 um, with a usual range of 6-8 um. In stained preparations, the nucleus has a distinct karysome that, while not as large as that seen in the trophozoite, is still larger than the karysome of the Entamoeba species. Peripheral chromatin is absent. Although the nuclei are not visible in unstained preparations, the karysomes are readily apparent in iodine-stained wet mounts. The cytoplasm may contain diffuse glycogen, and chromatid bodies are absent. Occasionally, small granules or inclusions may occur in the cytoplasm.

    TROPHOZOITES

    This stage is small, measuring 6-12 m, with an average range of 8-10 um. Living trophozoites are sluggish and generally non-progressive. The single nucleus sometimes is visible in unstained preparations. In stained organisms, the karyosome usually is large and irregularly shaped, but occasionally it may be fragmented or placed against one side of the nuclear membrane. There is no peripheral chromatin on the nuclear membrane. The cytoplasm, which is coarsely granular and often highly vacuolated, may contain bacteria.

    For more information view the source:Wikipedia

    << Back to Wiki

  • ENTAMOEBA COLI

    Although much literature cites this parasite as a non-pathogen, there is much reason to believe that in some cases these "non-pathogenic" agents actually cause symptoms in patients, with no other infections or conditions that would explain their symptoms. Following is a list of a few references to support that statement: Cuffari C, Oligny L, Siedman EG, 1998 Dientamoeba fragilis masquerading as allergic colitis. J. Pediatr Gastroenterol Nutr 26: 16-20. Feigin, RD, Cherry, James, Demmler-Harrison, GJ, and Kaplan, SL. Feigin and Cherry's Textbook of Pediatric Infectious Diseases, 6th Edition; Ch. 223, Amin, OM, 2002. Seasonal Prevalence of Intestinal Parasites in the United States During 2000. Am J. Trop. Med. Hyg., 66(6), 799-803., Garcia LS, 2005. Diagnostic Medical Parasitology. Washington, DC: American Society for Microbiology. Pg. 9

    BIOLOGY

    CAUSAL AGENTS

    Entamoeba coli, E. hartmanni, E. polecki, Endolimax nana, and Iodamoeba buetschlii are generally considered nonpathogenic and reside in the large intestine of the human host.  Entamoeba gingivalis is also considered nonpathogenic and resides in the oral cavity of the human host, in the gingival pockets at the base of the teeth.

    LIFE CYCLE (nonpathogenic intestinal amebae):

    Life cycle of nonpathogenic intestinal amebae

    Entamoeba coli, E. hartmanni, E. polecki, Endolimax nana, and Iodamoeba buetschlii are generally considered nonpathogenic and reside in the large intestine of the human host .  Both cysts and trophozoites of these species are passed in stool and considered diagnostic .  Cysts are typically found in formed stool, whereas trophozoites are typically found in diarrheal stool.  Colonization of the nonpathogenic amebae occurs after ingestion of mature cysts in fecally-contaminated food, water, or fomites .  Excystation occurs in the small intestine  and trophozoites are released, which migrate to the large intestine.  The trophozoites multiply by binary fission and produce cysts, and both stages are passed in the feces .  Because of the protection conferred by their cell walls, the cysts can survive days to weeks in the external environment and are responsible for transmission. Trophozoites passed in the stool are rapidly destroyed once outside the body, and if ingested would not survive exposure to the gastric environment.

    LIFE CYCLE (Entamoeba gingivalis):

    Life cycle of Entamoeba gingivalis

    There is no known cyst stage for Entamoeba gingivalis; trophozoites live in the oral cavity of humans, residing in the gingival pockets near the base of the teeth .  They are not considered pathogenic, and feed on bacteria and other debris.  Trophozoites are transmitted person-to-person orally by kissing or fomites (such as eating utensils) .  The trophozoite stage of E. gingivalis is morphologically similar to that of E. histolytica, and the two should be differentiated, as both can be coughed up in sputum specimens (for the latter, when present in pulmonary abscesses).

    GEOGRAPHIC DISTRIBUTION

    All six species are distributed worldwide.  Entamoeba polecki in nature is primarily a parasite of pigs and monkeys, and human infection is more prevalent in areas where the people have animal contact.

    CLINICAL FEATURES

    Entamoeba coli, E. hartmanni, E. polecki, Endolimax nana, and Iodamoeba buetschlii are generally considered nonpathogenic, although they have been found in the stool of patients presenting with diarrhea where no known pathogens were identified.  Their presence in stool can be an indicator of fecal contamination of a food or water source, and does not rule-out the presence of other parasites.  Entamoeba gingivalis is also considered nonpathogenic, but is found in about 95% of patients with gum disease and about 50% of patients with healthy gums.

    LABORATORY DIAGNOSIS

    For E. coli, E. hartmanni, E. polecki, E. nana, and I. buetschlii, identification is made by observing cysts and/or trophozoites in stool specimens, both concentrated wet mounts and permanent stained smears.  Identification of E. gingivalis is made by the finding of trophozoites in scrapings of the gums and teeth.  They may also be found in sputum in rare occasions.  As such, it is important to differentiate them from the morphologically-similar trophozoites of E. histolytica, which may be found in sputum from pulmonary abscesses.

    For more information view the source:Center for Disease Control

    <

  • ENTAMOEBA HARTMANNI

    Although much literature cites this parasite as a non-pathogen, there is much reason to believe that in some cases these "non-pathogenic" agents actually cause symptoms in patients, with no other infections or conditions that would explain their symptoms. Following is a list of a few references to support that statement: Cuffari C, Oligny L, Siedman EG, 1998 Dientamoeba fragilis masquerading as allergic colitis. J. Pediatr Gastroenterol Nutr 26: 16-20. Feigin, RD, Cherry, James, Demmler-Harrison, GJ, and Kaplan, SL. Feigin and Cherry's Textbook of Pediatric Infectious Diseases, 6th Edition; Ch. 223, Amin, OM, 2002. Seasonal Prevalence of Intestinal Parasites in the United States During 2000. Am J. Trop. Med. Hyg., 66(6), 799-803., Garcia LS, 2005. Diagnostic Medical Parasitology. Washington, DC: American Society for Microbiology. Pg. 9

     

    BIOLOGY

    CAUSAL AGENTS

    Entamoeba coli, E. hartmanni, E. polecki, Endolimax nana, and Iodamoeba buetschlii are generally considered nonpathogenic and reside in the large intestine of the human host.  Entamoeba gingivalis is also considered nonpathogenic and resides in the oral cavity of the human host, in the gingival pockets at the base of the teeth.

     

    LIFE CYCLE

    Life cycle of nonpathogenic intestinal amebae

    Entamoeba coli, E. hartmanni, E. polecki, Endolimax nana, and Iodamoeba buetschlii are generally considered nonpathogenic and reside in the large intestine of the human host .  Both cysts and trophozoites of these species are passed in stool and considered diagnostic .  Cysts are typically found in formed stool, whereas trophozoites are typically found in diarrheal stool.  Colonization of the nonpathogenic amebae occurs after ingestion of mature cysts in fecally-contaminated food, water, or fomites .  Excystation occurs in the small intestine  and trophozoites are released, which migrate to the large intestine.  The trophozoites multiply by binary fission and produce cysts, and both stages are passed in the feces .  Because of the protection conferred by their cell walls, the cysts can survive days to weeks in the external environment and are responsible for transmission. Trophozoites passed in the stool are rapidly destroyed once outside the body, and if ingested would not survive exposure to the gastric environment.

     

    LIFE CYCLE (Entamoeba gingivalis):

    Life cycle of Entamoeba gingivalis

    There is no known cyst stage for Entamoeba gingivalis; trophozoites live in the oral cavity of humans, residing in the gingival pockets near the base of the teeth .  They are not considered pathogenic, and feed on bacteria and other debris.  Trophozoites are transmitted person-to-person orally by kissing or fomites (such as eating utensils) .  The trophozoite stage of E. gingivalis is morphologically similar to that of E. histolytica, and the two should be differentiated, as both can be coughed up in sputum specimens (for the latter, when present in pulmonary abscesses).

     

    GEOGRAPHIC DISTRIBUTION

    All six species are distributed worldwide.  Entamoeba polecki in nature is primarily a parasite of pigs and monkeys, and human infection is more prevalent in areas where the people have animal contact.

     

    CLINICAL FEATURES

    Entamoeba coli, E. hartmanni, E. polecki, Endolimax nana, and Iodamoeba buetschlii are generally considered nonpathogenic, although they have been found in the stool of patients presenting with diarrhea where no known pathogens were identified.  Their presence in stool can be an indicator of fecal contamination of a food or water source, and does not rule-out the presence of other parasites.  Entamoeba gingivalis is also considered nonpathogenic, but is found in about 95% of patients with gum disease and about 50% of patients with healthy gums.

     

    LABORATORY DIAGNOSIS

    For E. coli, E. hartmanni, E. polecki, E. nana, and I. buetschlii, identification is made by observing cysts and/or trophozoites in stool specimens, both concentrated wet mounts and permanent stained smears.  Identification of E. gingivalis is made by the finding of trophozoites in scrapings of the gums and teeth.  They may also be found in sputum in rare occasions.  As such, it is important to differentiate them from the morphologically-similar trophozoites of E. histolytica, which may be found in sputum from pulmonary abscesses.

    For more information view the source:Center for Disease Control

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  • ENTAMOEBA HISTOLYTICA

    Entamoeba histolytica is an anaerobic parasitic protozoan, part of the genus Entamoeba. Predominantly infecting humans and other primates, E. histolytica is estimated to infect about 50 million people worldwide. Previously, it was thought that 10% of the world population was infected, but these figures predate the recognition that at least 90% of these infections were due to a second species, E. dispar. Mammals such as dogs and cats can become infected transiently, but are not thought to contribute significantly to transmission.

    FAQs

    What is amebiasis?

    Amebiasis is a disease caused by a one-celled parasite called Entamoeba histolytica.

    Who is at risk for amebiasis?

    Although anyone can have this disease, it is more common in people who live in tropical areas with poor sanitary conditions. In the United States, amebiasis is most common in:

    • People who have traveled to tropical places that have poor sanitary conditions
    • Immigrants from tropical countries that have poor sanitary conditions
    • People who live in institutions that have poor sanitary conditions
    • Men who have sex with men

    How can I become infected with E. histolytica?

    E. histolytica infection can occur when a person:

    • Puts anything into their mouth that has touched the feces of a person who is infected with E. histolytica.
    • Swallows something, such as water or food, that is contaminated with E. histolytica.
    • Swallows E. histolytica cysts (eggs) picked up from contaminated surfaces or fingers.

    What are the symptoms of amebiasis?

    Only about 10% to 20% of people who are infected with E. histolytica become sick from the infection. The symptoms are often quite mild and can include loose feces (poop), stomach pain, and stomach cramping. Amebic dysentery is a severe form of amebiasis associated with stomach pain, bloody stools , and fever. Rarely, E. histolytica invades the liver and forms an abscess (a collection of pus). In a small number of instances, it has been shown to spread to other parts of the body, such as the lungs or brain, but this is very uncommon.

    If I swallowed E. histolytica, how quickly would I become sick?

    Only about 10% to 20% of people who are infected with E. histolytica become sick from the infection. Those people who do become sick usually develop symptoms within 2 to 4 weeks, though it can sometimes take longer.

    What should I do if I think I have amebiasis?

    See your health care provider.

    How is amebiasis diagnosed?

    Your health care provider will ask you to submit fecal samples. Because E. histolytica is not always found in every stool sample, you may be asked to submit several stool samples from several different days.

    Diagnosis of amebiasis can be very difficult. One problem is that other parasites and cells can look very similar to E. histolytica when seen under a microscope. Therefore, sometimes people are told that they are infected with E. histolytica even though they are not. Entamoeba histolytica and another ameba, Entamoeba dispar, which is about 10 times more common, look the same when seen under a microscope. Unlike infection with E. histolytica, which sometimes makes people sick, infection with E. dispar does not make people sick and therefore does not need to be treated.

    If you have been told that you are infected with E. histolytica but you are feeling fine, you might be infected with E. dispar instead. Unfortunately, most laboratories do not yet have the tests that can tell whether a person is infected with E. histolytica or with E. dispar. Until these tests become more widely available, it usually is best to assume that the parasite is E. histolytica.

    A blood test is also available but is only recommended when your health care provider thinks that your infection may have spread beyond the intestine (gut) to some other organ of your body, such as the liver. However, this blood test may not be helpful in diagnosing your current illness because the test can be positive if you had amebiasis in the past, even if you are no longer infected now.

    How is amebiasis treated?

    Several antibiotics are available to treat amebiasis. Treatment must be prescribed by a physician. You will be treated with only one antibiotic if your E. histolytica infection has not made you sick. You probably will be treated with two antibiotics (first one and then the other) if your infection has made you sick.

    I am going to travel to a country that has poor sanitary conditions. What should I eat and drink there so I will NOT become infected with E. histolytica or other such germs?

    The following items are safe to drink:

    • Bottled water
    • Tap water that has been boiled for at least 1 minute
    • Carbonated (bubbly) water from sealed cans or bottles
    • Carbonated (bubbly) drinks (like soda) from sealed cans or bottles

    *You can also make tap water safe for drinking by filtering it through an "absolute 1 micron or less" filter and dissolving chlorine, chlorine dioxide, or iodine tablets in the filtered water. "Absolute 1 micron" filters can be found in camping/outdoor supply stores.

    The following items are NOT safe to drink or eat:

    • Fountain drinks or any drinks with ice cubes
    • Fresh fruit or vegetables that you did not peel yourself
    • Milk, cheese, or dairy products that may not have been pasteurized.
    • Anything sold by street vendors

    Should I be concerned about spreading the infection to others?

    Yes, but the risk of spreading infection is low if the infected person is treated with antibiotics and practices good personal hygiene. This includes thorough handwashing with soap and warm water after using the toilet, after changing diapers, and before handling food.

    BIOLOGY

    Causal Agent:

    Several protozoan species in the genus Entamoeba colonize humans, but not all of them are associated with disease. Entamoeba histolytica is well recognized as a pathogenic ameba, associated with intestinal and extraintestinal infections. The other species are important because they may be confused with E. histolytica in diagnostic investigations.

    Life Cycle

    Life Cycle of Entamoeba histolyticaCysts and trophozoites are passed in feces . Cysts are typically found in formed stool, whereas trophozoites are typically found in diarrheal stool. Infection by Entamoeba histolytica occurs by ingestion of mature cysts in fecally contaminated food, water, or hands. Excystation occurs in the small intestine and trophozoites are released, which migrate to the large intestine. The trophozoites multiply by binary fission and produce cysts , and both stages are passed in the feces . Because of the protection conferred by their walls, the cysts can survive days to weeks in the external environment and are responsible for transmission. Trophozoites passed in the stool are rapidly destroyed once outside the body, and if ingested would not survive exposure to the gastric environment. In many cases, the trophozoites remain confined to the intestinal lumen (noninvasive infection) of individuals who are asymptomatic carriers, passing cysts in their stool. In some patients the trophozoites invade the intestinal mucosa (intestinal disease), or, through the bloodstream, extraintestinal sites such as the liver, brain, and lungs (extraintestinal disease), with resultant pathologic manifestations. It has been established that the invasive and noninvasive forms represent two separate species, respectively E. histolytica and E. dispar. These two species are morphologically indistinguishable unless E. histolytica is observed with ingested red blood cells (erythrophagocystosis). Transmission can also occur through exposure to fecal matter during sexual contact (in which case not only cysts, but also trophozoites could prove infective).

    Life cycle image and information courtesy of DPDx.

    For more information view the source:Center for Disease Control

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  • ENTEROBIUS VERMICULARIS

    Pinworm infection is caused by a small, thin, white roundworm called Enterobius vermicularis. Although pinworom infection can affect all people, it most commonly occurs among children, institutionalized persons, and household members of persons with pinworm infection. Pinworm infection is treatable with over-the-counter or prescription medication, but reinfection, which occurs easily, should be prevented.

    FAQS

    What is a pinworm?

    A pinworm ("threadworm") is a small, thin, white roundworm (nematode) called Enterobius vermicularis that sometimes lives in the colon and rectum of humans. Pinworms are about the length of a staple. While an infected person sleeps, female pinworms leave the intestine through the anus and deposit their eggs on the surrounding skin.

    What are the symptoms of a pinworm infection?

    Pinworm infection (called enterobiasis or oxyuriasis) causes itching around the anus which can lead to difficulty sleeping and restlessness. Symptoms are caused by the female pinworm laying her eggs. Symptoms of pinworm infection usually are mild and some infected people have no symptoms.

    Who is at risk for pinworm infection?

    Pinworm infection occurs worldwide and affects persons of all ages and socioeconomic levels. It is the most common worm infection in the United States. Pinworm infection occurs most commonly among:

    • school-aged and preschool-aged children,
    • institutionalized persons, and
    • household members and caretakers of persons with pinworm infection.

    Pinworm infection often occurs in more than one person in household and institutional settings. Child care centers often are the site of cases of pinworm infection.

    How is pinworm infection spread?

    Pinworm infection is spread by the fecal-oral route, that is by the transfer of infective pinworm eggs from the anus to someone’s mouth, either directly by hand or indirectly through contaminated clothing, bedding, food, or other articles.

    Pinworm eggs become infective within a few hours after being deposited on the skin around the anus and can survive for 2 to 3 weeks on clothing, bedding, or other objects. People become infected, usually unknowingly, by swallowing (ingesting) infective pinworm eggs that are on fingers, under fingernails, or on clothing, bedding, and other contaminated objects and surfaces. Because of their small size, pinworm eggs sometimes can become airborne and ingested while breathing.

    Can my family become infected with pinworms from swimming pools?

    Pinworm infections are rarely spread through the use of swimming pools. Pinworm infections occur when a person swallows pinworm eggs picked up from contaminated surfaces or fingers. Although chlorine levels found in pools are not high enough to kill pinworm eggs, the presence of a small number of pinworm eggs in thousands of gallons of water (the amount typically found in pools) makes the chance of infection unlikely.

    My little kids like to co-bathe, could this be how they are becoming infected?

    During this treatment time and two weeks after final treatment, it is a good idea to avoid co-bathing and the reuse or sharing of washcloths. Showering may be preferred to avoid possible contamination of bath water. Careful handling and frequent changing of underclothing, night clothes, towels, and bedding can help reduce infection, reinfection, and environmental contamination with pinworm eggs. These items should be laundered in hot water, especially after each treatment of the infected person and after each usage of washcloths until infection is cleared.

    Did my pets give me pinworms / can I give pinworms to my pets?

    No. Humans are considered to be the only hosts of E. vermicularis which is also known as the human pinworm.

    How is pinworm infection diagnosed?

    Itching during the night in a childs perianal area strongly suggests pinworm infection. Diagnosis is made by identifying the worm or its eggs. Worms can sometimes be seen on the skin near the anus or on underclothing, pyjamas, or sheets about 2 to 3 hours after falling asleep.

    Pinworm eggs can be collected and examined using the tape test as soon as the person wakes up. This is done by firmly pressing the adhesive side of clear, transparent cellophane tape to the skin around the anus. The eggs stick to the tape and the tape can be placed on a slide and looked at under a microscope. Because washing/bathing or having a bowel movement can remove eggs from the skin, this test should be done as soon as the person wakes up in the morning before they wash, bathe, go to the toilet, or get dressed. The “tape test� should be done on three consecutive mornings to increase the chance of finding pinworm eggs.

    Because itching and scratching of the anal area is common in pinworm infection, samples taken from under the fingernails may also contain eggs. Pinworm eggs rarely are found in routine stool or urine samples.

    How is pinworm infection treated?

    Pinworm can be treated with either prescription or over-the-counter medications. A health care provider should be consulted before treating a suspected case of pinworm infection.

    Treatment involves two doses of medication with the second dose being given 2 weeks after the first dose. All household contacts and caretakers of the infected person should be treated at the same time. Reinfection can occur easily so strict observance of good hand hygiene is essential (e.g. proper handwashing, maintaining clean short fingernails, avoiding nail biting, avoiding scratching the perianal area).

    Daily morning bathing and daily changing of underwear helps removes a large proportion of eggs. Showering may be preferred to avoid possible contamination of bath water. Careful handling and frequent changing of underclothing, night clothes, towels, and bedding can help reduce infection, reinfection, and environmental contamination with pinworm eggs. These items should be laundered in hot water, especially after each treatment of the infected person and after each usage of washcloths until infection is cleared.

    Should family and other close contacts of someone with pinworm also be treated for pinworm?

    Yes. The infected person and all household contacts and caretakers of the infected person should be treated at the same time.

    What should be done if the pinworm infection occurs again?

    Reinfection occurs easily. Prevention always should be discussed at the time of treatment. Good hand hygiene is the most effective means of prevention. If pinworm infection occurs again, the infected person should be retreated with the same two-dose treatment. The infected person’s household contacts and caretakers also should be treated. If pinworm infection continues to occur, the source of the infection should be sought and treated. Playmates, schoolmates, close contacts outside the home, and household members should be considered possible sources of infection. Each infected person should receive the recommended two-dose treatment.

    How can pinworm infection and reinfection be prevented?

    Strict observance of good hand hygiene is the most effective means of preventing pinworm infection. This includes washing hands with soap and warm water after using the toilet, changing diapers, and before handling food. Keep fingernails clean and short, avoid fingernail-biting, and avoid scratching the skin in the perianal area. Teach children the importance of washing hands to prevent infection.

    Daily morning bathing and changing of underclothes helps remove a large proportion of pinworm eggs and can help prevent infection and reinfection. Showering may be preferred to avoid possible contamination of bath water. Careful handling (avoid shaking) and frequent laundering of underclothes, night clothes, towels, and bed sheets using hot water also helps reduce the chance of infection and reinfection by reducing environmental contamination with eggs.

    Control can be difficult in child care centers and schools because the rate of reinfection is high. In institutions, mass and simultaneous treatment, repeated in 2 weeks, can be effective. Hand hygiene is the most effective method of prevention. Trimming and scrubbing the fingernails and bathing after treatment is important to help prevent reinfection and spread of pinworms.

    EPIDEMIOLOGY & RISK FACTORS

    Pinworm infections are more common within families with school-aged children, in primary caregivers of infected children, and in institutionalized children.

    A person is infected with pinworms by ingesting pinworm eggs either directly or indirectly. These eggs are deposited around the anus by the worm and can be carried to common surfaces such as hands, toys, bedding, clothing, and toilet seats. By putting anyones contaminated hands (including ones own) around the mouth area or putting ones mouth on common contaminated surfaces, a person can ingest pinworm eggs and become infected with the pinworm parasite. Since pinworm eggs are so small, it is possible to ingest them while breathing.

    Once someone has ingested pinworm eggs, there is an incubation period of 1 to 2 months or longer for the adult gravid female to mature in the small intestine. Once mature, the adult female worm migrates to the colon and lays eggs around the anus at night, when many of their hosts are asleep. People who are infected with pinworm can transfer the parasite to others for as long as there is a female pinworm depositing eggs on the perianal skin. A person can also re-infect themselves, or be re-infected by eggs from another person.

    The people most likely to be infected with pinworm are children under 18, people who take care of infected children and people who are institutionalized. In these groups, the prevalence can reach 50%.

    Pinworm is the most common worm infection in the United States. Humans are the only species that can transfer this parasite. Household pets like dogs and cats cannot become infected with human pinworms. Pinworm eggs can survive in the indoor environment for 2 to 3 weeks.

    BIOLOGY

    Causal Agent:

    The nematode (roundworm) Enterobius vermicularis (previously Oxyuris vermicularis) also called human pinworm. (Adult females: 8 to 13 mm, adult male: 2 to 5 mm. )Â Humans are considered to be the only hosts of E. vermicularis. A second species, Enterobius gregorii, has been described and reported from Europe, Africa, and Asia. For all practical purposes, the morphology, life cycle, clinical presentation, and treatment of E. gregorii is identical to E. vermicularis.

    Life Cycle:

    Life Cycle of Enterobius vermicularis

    Eggs are deposited on perianal folds. Self-infection occurs by transferring infective eggs to the mouth with hands that have scratched the perianal area. Person-to-person transmission can also occur through handling of contaminated clothes or bed linens. Enterobiasis may also be acquired through surfaces in the environment that are contaminated with pinworm eggs (e.g. , curtains, carpeting). Some small number of eggs may become airborne and inhaled. These would be swallowed and follow the same development as ingested eggs. Following ingestion of infective eggs, the larvae hatch in the small intestine and the adults establish themselves in the colon. The time interval from ingestion of infective eggs to oviposition by the adult females is about one month. The life span of the adults is about two months. Gravid females migrate nocturnally outside the anus and oviposit while crawling on the skin of the perianal area. The larvae contained inside the eggs develop (the eggs become infective) in 4 to 6 hours under optimal conditions. Retroinfection, or the migration of newly hatched larvae from the anal skin back into the rectum, may occur but the frequency with which this happens is unknown.

    Life cycle image and information courtesy of DPDx.

    DISEASE

    The most common clinical manifestation of a pinworm infection is an itchy anal region. When the infection is heavy, there can be a secondary bacterial infection due to the irritation and scratching of the anal area. Often the patient will complain of teeth grinding, and insomnia due to disturbed sleep, or even abdominal pain or appendicitis. Infection of the female genital tract has been well reported.

    DIAGNOSIS

    A person infected with pinworm is often asymptomatic, but itching around the anus is a common symptom. Diagnosis of pinworm can be reached from three simple techniques. The first option is to look for the worms in the perianal reqion 2 to 3 hours after the infected person is asleep. The second option is to touch the perianal skin with transparent tape to collect possible pinworm eggs around the anus first thing in the morning. If a person is infected, the eggs on the tape will be visible under a microscope. The tape method should be conducted on 3 consecutive mornings right after the infected person wakes up and before he/she does any washing. Since anal itching is a common symptom of pinworm, the third option for diagnosis is analyzing samples from under fingernails under a microscope. An infected person who has scratched the anal area may have picked up some pinworm eggs under the nails that could be used for diagnosis.

    Since pinworm eggs and worms are often sparse in stool, examining stool samples is not recommended. Serologic tests are not available for diagnosing pinworm infections.

    PREVENTION AND CONTROL

    Washing your hands with soap and warm water after using the toilet, changing diapers, and before handling food is the most successful way to prevent pinworm infection. In order to stop the spread of pinworm and possible re-infection, people who are infected should bathe every morning to help remove a large amount of the eggs on the skin. Showering is a better method than taking a bath, because showering avoids potentially contaminating the bath water with pinworm eggs. Infected people should not co-bathe with others during their time of infection.

    Also, infected people should comply with good hygiene practices such as washing their hands with soap and warm water after using the toilet, changing diapers, and before handling food. They should also cut fingernails regularly, and avoid biting the nails and scratching around the anus. Frequent changing of underclothes and bed linens first thing in the morning is a great way to prevent possible transmission of eggs in the environment and risk of reinfection. These items should not be shaken and carefully placed into a washer and laundered in hot water followed by a hot dryer to kill any eggs that may be there.

    In institutions, day care centers, and schools, control of pinworm can be difficult, but mass drug administration during an outbreak can be successful. Teach children the importance of washing hands to prevent infection.

    For more information view the source:Center for Disease Control

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  • FASCIOLA

    Fascioliasis is a parasitic infection typically caused by Fasciola hepatica, which is also known as "the common liver fluke" or "the sheep liver fluke." A related parasite, Fasciola gigantica, also can infect people. Fascioliasis is found in all 5 continents, in over 50 countries, especially where sheep or cattle are reared. People usually become infected by eating raw watercress or other water plants contaminated with immature parasite larvae. The immature larval flukes migrate through the intestinal wall, the abdominal cavity, and the liver tissue, into the bile ducts, where they develop into mature adult flukes, which produce eggs. The pathology typically is most pronounced in the bile ducts and liver. Fasciola infection is both treatable and preventable.

     

    FAQS

    What is fascioliasis?

    Fascioliasis is an infectious  disease caused by Fasciola parasites,  which are flat worms referred to as liver flukes. The adult (mature) flukes are  found in the bile ducts and liver of infected people and animals, such as sheep  and cattle. In general, fascioliasis is more common in livestock and other  animals than in people.

    Two Fasciola species (types) infect people. The main species is Fasciola hepatica, which is also known  as "the common liver fluke" and "the sheep liver fluke." A related species, Fasciola gigantica, also can infect people.

     

    In what parts of the world is fascioliasis found?

    Fascioliasis is found in more  than 50 countries, especially where sheep or cattle are reared. Fasciola hepatica is found in all continents  except Antarctica. Fasciola gigantica has been found in some tropical areas. Except for parts of Western Europe,  human fascioliasis has mainly been documented in developing countries.

     

    How do people get infected with Fasciola?

    People get infected by accidentally  ingesting (swallowing) the parasite. The main way this happens is by eating raw  watercress or other contaminated freshwater plants. People also can get  infected by ingesting contaminated water, such as by drinking it or by eating  vegetables that were washed or irrigated with contaminated water.

     

    Can Fasciola be spread directly from one person (or animal) to another?

    No. Fasciola cannot be passed directly from one person to another. The eggs passed in the  stool of infected people (and animals) need to develop (mature) in certain types  of freshwater snails, under favorable environmental conditions, to be able to  infect someone else.

    Under unusual circumstances, people have gotten infected by eating undercooked sheep or goat liver that contained immature forms of the  parasite.

     

    Can people get infected with Fasciola in the United States?

    Yes. It is possible, but few  cases have been reported in published articles.

    Approximately 20 cases in Hawaii  over a several-decade period were described in articles in the 1950s. One case  in Florida and at least one case in California linked to watercress have been reported.

    However, most reported cases  in the United States have been in people, such as immigrants, who were infected  in countries where fascioliasis is well known to occur.

     

    What are the signs and symptoms of Fasciola infection, and when do they begin?

    Some infected people don't  ever feel sick.

    Some people feel sick early  on in the infection, while immature flukes are passing (migrating) from the  intestine through the abdominal cavity and liver. Symptoms from the acute  (migratory) phase can start 4 to 7 days after the exposure and can last several  weeks or months.

    Some people feel sick during  the chronic phase of the infection, when adult flukes are in the bile ducts (the  duct system of the liver). The symptoms, if any, associated with this phase can  start months to years after the exposure. For example, symptoms can result from  inflammation and blockage of bile ducts.

    During  both phases of infection, clinical features can include fever, malaise, abdominal  pain, eosinophilia, hepatomegaly (an enlarged liver), and abnormal liver tests.

     

    What should people do if they think they might be infected with Fasciola?

    See their health care provider.

     

    How is Fasciola infection diagnosed?

    The infection typically is diagnosed by examining stool  (fecal) specimens under a microscope. The diagnosis is confirmed if Fasciola eggs are seen. More than one  specimen may need to be examined to find the parasite. Certain types of blood  tests also may be helpful for diagnosing Fasciola infection.

     

    Can fascioliasis be treated?

    Yes.  Fascioliasis is a treatable disease. Triclabendazole is the drug of choice. It is  given by mouth, usually in one or two doses. Most people respond well to the  treatment.

     

    How can Fasciola infection be prevented?

    People can protect  themselves by not eating raw watercress and other water plants, especially from  endemic grazing areas. As always, travelers to areas with poor sanitation  should avoid food and water that might be contaminated. No vaccine is  available to protect people against Fasciola.

     

    EPIDEMIOLOGY & RISK FACTORS

    Fascioliasis occurs in many areas of the world and usually  is caused by F. hepatica, which is a  common liver fluke of sheep and cattle. In general, animal fascioliasis is more  common and widespread than human fascioliasis. Even so, the estimated number of  infected people is at least 2.4 million and might be as high as 17 million.

    Fasciola  hepatica is  found in more than 50 countries, in all continents except Antarctica. It is  found in parts of Latin America, the Caribbean, Europe, the Middle East,  Africa, Asia, and Oceania. Fasciola  gigantica is less widespread. Human cases have been reported in the  tropics, in parts of Africa and Asia and also in Hawaii.

    In some areas where fascioliasis is found, human cases are  uncommon (sporadic). In other areas, human fascioliasis is very common (hyperendemic).  For example, the areas with the highest known rates of human infection are in  the Andean highlands of Bolivia and Peru.

    Special conditions are needed for fascioliasis to be present  in an area, and its geographic distribution is very patchy (focal). The  eggs passed in the stool of infected mammals have to develop (mature) in a suitable  aquatic snail host to be able to infect another mammalian host. Requirements  include sufficient moisture and favorable temperatures (above 50°F) that allow  the development of miracidia, reproduction of snails, and larval development  within the snails. These factors also contribute to both the prevalence and level (intensity) of infection.  Prevalence is highest in areas where climatic conditions promote development of  cercariae.

    Infective Fasciola larvae (metacercariae) are  found in contaminated water, either stuck to (encysted on) water plants or  floating in the water, often in marshy areas, ponds, or flooded pastures. People  (and animals) typically become infected by eating raw watercress or other  contaminated water plants. The plants may be eaten as a snack or in salads or  sandwiches. People also can get infected by ingesting contaminated water, such  as by drinking it or by eating vegetables that were washed or irrigated with contaminated water. Infection also can result from eating undercooked sheep or goat livers  that contain immature forms of the parasite.

    The possibility of becoming  infected in the United States should be considered, despite the fact that few  locally acquired cases have been documented. The prerequisites for the Fasciola life cycle exist in some parts  of the United States. In addition, transmission because of imported  contaminated produce could occur, as has been documented in Europe.

     

    BIOLOGY

    Casual Agent:

    Fascioliasis is caused by Fasciola hepatica and less often by F. gigantica, which are flat worms classified  as liver flukes (trematodes). Some human cases have been caused by hybrid  species. Additional Fasciola species  have been found in animals.

     

    Life Cycle:

    As shown below, Fasciola parasites develop into adult  flukes in the bile ducts of infected mammals, which pass immature Fasciola eggs in their feces. The next  part of the life cycle occurs in freshwater. After several weeks, the eggs  hatch, producing a parasite form known as the miracidium, which then infects a snail  host. Under optimal conditions, the development process in the snail may be  completed in 5 to 7 weeks; cercariae are then shed in the water around the  snail. The cercariae lose their tails when they encyst as metacercariae  (infective larvae) on water plants. In contrast to cercariae, metacercariae have  a hard outer cyst wall and can survive for prolonged periods in wet environments.

     

    Life Cycle of Schistomes

    Immature Fasciola eggs are discharged in the biliary ducts and in the stool. Eggs become embryonated in water, eggs release miracidiawhich invade a suitable snail intermediate host, including the genera Galba, Fossaria and Pseudosuccinea. In the snail the parasites undergo several developmental stages (sporocysts). The cercariae are released from the snail and encyst as metacercariae on aquatic vegetation or other surfaces. Mammals acquire the infection by eating vegetation containing metacercariae. Humans can become infected by ingesting metacercariae-containing freshwater plants, especially watercress. After ingestion, the metacercariae excyst in the duodenum and migrate through the intestinal wall, the peritoneal cavity, and the liver parenchyma into the biliary ducts, where they develop into adult flukes.

    In humans, maturation from metacercariae into adult flukes takes approximately 3 to 4 months. The adult flukes (Fasciola hepatica: up to 30 mm by 13 mm; F. gigantica: up to 75 mm) reside in the large biliary ducts of the mammalian host. Fasciola hepatica infect various animal species, mostly herbivores (plant-eating animals).

    Life cycle image and information courtesy of DPDx.

     

    DISEASE

    Human fascioliasis is usually recognized as an infection of  the bile ducts and liver, but infection in other parts of the body can occur.

    In the early (acute) phase, symptoms can occur as a result  of the parasite's migration from the intestine to and through the liver.  Symptoms can include gastrointestinal problems such as nausea, vomiting, and  abdominal pain/tenderness. Fever, rash, and difficulty breathing may occur.

    During the chronic phase (after the parasite settles in the  bile ducts), the clinical manifestations may be similar or more discrete, reflecting inflammation and blockage of bile  ducts, which can be intermittent. Inflammation of the liver, gallbladder, and  pancreas also can occur.

     

    DIAGNOSIS

    The standard  way to be sure a person is infected with Fasciola is by seeing the parasite. This is usually done by finding Fasciola eggs in stool (fecal) specimens  examined under a microscope. More than one specimen may need to be examined to  find the parasite. Sometimes eggs are found by examining duodenal contents or  bile.

    Infected people don't start  passing eggs until they have been infected for several months; people don't pass  eggs during the acute phase of the infection. Therefore, early on, the  infection has to be diagnosed in other ways than by examining stool. Even  during the chronic phase of infection, it can be difficult to find eggs in  stool specimens from people who have light infections.

    Certain types of blood tests can  be helpful for diagnosing Fasciola infection,  including routine blood work and tests that detect antibodies (an immune  response) to the parasite.

     

    PREVENTION AND CONTROL

    No vaccine is available to protect people against Fasciola infection.

    In some areas of the world where  fascioliasis is found (endemic), special control programs are in place or are planned.  The types of control measures depend on the setting (such as epidemiologic,  ecologic, and cultural factors). Strict control of the growth and sale of  watercress and other edible water plants is important.

    Individual people can protect  themselves by not eating raw watercress and other water plants, especially from  endemic grazing areas. As always, travelers to areas with poor sanitation  should avoid food and water that might be contaminated (tainted). Vegetables  grown in fields that might have been irrigated with polluted water should be  thoroughly cooked, as should viscera from potentially infected animals.

    For more information view the source:Center for Disease Control

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  • GIARDIA

    Giardia is a genus of anaerobic flagellated protozoan parasites of the phylum Diplomonada in the supergroup "Excavata" (named for the excavated groove on one side of the cell body) that colonise and reproduce in the small intestines of several vertebrates, causing giardiasis. Their life cycle alternates between an actively swimming trophozoite and an infective, resistant cyst. The genus was named after French zoologist Alfred Mathieu Giard.

    CHARACTERISTICS

    Like other diplomonads, Giardia have two nuclei, each with four associated flagella, and lack both mitochondria and a Golgi apparatus. However they are now known to possess mitochondrial relics, called mitosomes. These are not used in ATP synthesis the way mitochondria are, but are involved in the maturation of iron-sulfur proteins. The synapomorphies of genus Giardia include cells with duplicate organelles, absence of cytostomes, and ventral adhesive disc.

    INFECTION AND SYMPTOMS

    Giardia lives inside the intestines of infected humans or other animals. Individuals become infected through ingesting or coming into contact with contaminated food, soil, or water. The Giardia parasite originates from contaminated items and surfaces that have been tainted by the feces of an infected animal. The symptoms of Giardia, which may begin to appear 2 days after infection, include violent diarrhea, excess gas, stomach or abdominal cramps, upset stomach, and nausea. Resulting dehydration and nutritional loss may need immediate treatment. After 1-2 days of diarrhea, the opposite occurs, constipation for 4-7 days, still with acute gas production. The typical infection within an individual can be slight, resolve without treatment, and last between 2–6 weeks, although sometimes longer and/or more severe. Coexistence with the parasite is possible, symptoms fade, but one can remain a carrier and transmit it to others. Medication containing tinidazole or metronidazole decreases symptoms and time to resolution, albendazole is also used and has an anti-helmintic (anti-worm) property as well, ideal for certain compounded issues when a general vermicidal agent is preferred.

    PREVENTION

    Person-to-person transmission accounts for a majority of Giardia infections and is usually associated with poor hygiene and sanitation. Water-borne transmission is associated with the ingestion of contaminated water. In the U.S. outbreaks typically occur in small water systems using inadequately treated surface water. Venereal transmission happens through fecal-oral contamination. Additionally, diaper changing and inadequate hand washing are risk factors for transmission from infected children. Lastly, food-borne epidemics of Giardia have developed through the contamination of food by infected food-handlers.

    GENOME

    A Giardia isolate (WB) was the first diplomonad to have its genome sequenced. Its 11.7 million basepair genome is compact in structure and content with simplified basic cellular machineries and metabolism. Currently the genomes of several other Giardia isolates and diplomonads (the fish pathogens Spironucleus vortens and S. salmonicida) are being sequenced. A second isolate (the B assemblage) from humans has been sequenced along with a species from a pig (the E assemblage). There are 5000 genes in the genome. The E assemblage is more closely related to the A assemblage than is the B. A number of chromosomal rearrangements are present.

    For more information view the source:Wikipedia

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  • GIARDIA LAMBLIA

    Giardia is a microscopic parasite that causes the diarrheal illness known as giardiasis. Giardia (also known as Giardia intestinalis, Giardia lamblia, or Giardia duodenalis) is found  on surfaces or in soil, food, or water that has been contaminated with feces  from infected humans or animals.

    Giardia is protected by an outer shell that allows it to survive outside the body for long periods of time and makes it tolerant to chlorine disinfection. While the parasite can be spread in different ways, water (drinking water and recreational water) is the most common method of transmission.

     

    FAQS

    What is giardiasis?

    Giardiasis is a diarrheal disease caused  by the microscopic parasite Giardia. A parasite is an organism that  feeds off of another to survive. Once a person or animal (for example,  cats, dogs, cattle, deer, and beavers) has been  infected with Giardia, the parasite lives in the intestines and is  passed in feces . Once outside the body, Giardia can sometimes survive for weeks or months.  Giardia can be found within every region of the  U.S. and around the world.

    How do you get giardiasis and how is it spread?

    Giardiasis can be spread by:

    • Swallowing Giardia picked up from surfaces (such as bathroom handles, changing tables, diaper pails, or toys) that contain stool from an infected person or animal
    • Drinking water or using ice made from water sources where Giardia may live (for example, untreated  or improperly treated water from lakes, streams, or wells)
    • Swallowing water while swimming or playing in water where Giardia may live, especially in lakes, rivers, springs, ponds, and streams
    • Eating uncooked food that contains Giardia organisms
    • Having  contact with someone who is ill with giardiasis
    • Traveling to countries where giardiasis is common

    Anything that comes into contact with feces from infected  humans or animals can become contaminated with the Giardia parasite. People become infected when they swallow the parasite. It is not possible to become infected through contact with blood.

    What are the symptoms of giardiasis?

    infection can cause a variety of intestinal symptoms, which include:

    • Diarrhea
    • Gas or flatulence
    • Greasy stool that can float
    • Stomach or abdominal cramps
    • Upset stomach or nausea
    • Dehydration

    These symptoms may also lead to weight loss. Some  people with Giardia infection have no symptoms at all.

    How long after infection do symptoms  appear?

    Symptoms of giardiasis normally begin 1 to 3 weeks after becoming infected.

    How long will symptoms last?

    In otherwise  healthy people, symptoms of giardiasis may last 2 to 6 weeks. Occasionally,  symptoms last longer. Medications can help decrease the amount of time symptoms  last.

    Who is most at risk of getting giardiasis?

    Though giardiasis is commonly thought of as a camping or backpacking-related disease and is sometimes called "Beaver Fever," anyone  can get giardiasis. People more likely to become infected include:

    • Children  in child care settings, especially diaper-aged children
    • Close contacts (for example, people living in the same  household) or people who care for those sick with giardiasis
    • People who drink water or use ice made from places where Giardia may live (for example, untreated or  improperly treated water from lakes, streams, or wells)
    • Backpackers, hikers, and campers who drink unsafe water or who do not practice good hygiene (for example, proper handwashing)
    • People who swallow water while swimming and playing in  recreational water where Giardia may  live, especially in lakes, rivers, springs, ponds, and streams
    • International travelers
    • People exposed to human feces through sexual contact

    What should I do if I think I may  have giardiasis?

    Contact your health care provider.

    How is a giardiasis diagnosed?

    Your health care provider will ask you to submit stool samples to see if you are infected. Because testing for giardiasis can be difficult, you may be asked to submit several stool specimens collected over several days.

    What is the treatment for giardiasis?

    Many  prescription drugs are available to treat giardiasis. Although the Giardia parasite can infect all people, infants and pregnant women may be more likely to experience dehydration from the diarrhea caused by giardiasis. To prevent dehydration, infants and pregnant women should drink a lot of fluids while ill. Dehydration can be life threatening for infants, so it is especially important that parents talk to their health care providers about treatment options for their infants.

    My child does not have diarrhea, but was recently diagnosed as having Giardia infection. My health care provider says treatment is not necessary. Is this correct?

    Your child does not usually need  treatment if he or she has no symptoms. However, there are a few exceptions.  If your child does not have diarrhea, but does have other symptoms such as  nausea or upset stomach, tiredness, weight loss, or a lack of hunger, you and  your health care provider may need to think about treatment. The same is true  if many family members are ill, or if a family member is pregnant and unable to  take the most effective medications to treat Giardia. Contact your health care provider for specific treatment recommendations.

    If my water comes from a well, should I have my well water tested?

    Giardia and Well Water Testing

    What can I do to Prevent and Control giardiasis?

    To prevent and control infection with the parasite, it is important to:

    • Practice  good hygiene
    • Avoid  water (drinking or recreational) that may be contaminated
    • Avoid  eating food that may be contaminated
    • Prevent contact and contamination with feces  during sex

     

    EPIDEMIOLOGY & RISK FACTORS

    Giardiasis is a diarrheal illness caused by the parasite Giardia  intestinalis (also known as Giardia lamblia or Giardia  duodenalis). A parasite is an  organism that feeds off of another to survive.

    Giardiasis is a global disease. It infects nearly 2% of adults and  6% to 8% of children in developed countries worldwide. Nearly 33% of people in developing countries have had giardiasis. In the United States, Giardia infection is the most common intestinal parasitic disease affecting humans.

    People become infected with Giardia by swallowing Giardia cysts (hard shells containing Giardia) found in contaminated food or water. Cysts are instantly infectious once they leave the host through feces. An infected person might shed 1-10 billion cysts daily in their feces  and this might last for several months.  However, swallowing as few as 10 cysts might cause someone to become. Giardia may be passed person-to-person or even animal-to-person. Also, oral-anal contact during sex has been known to cause infection.  Symptoms of giardiasis normally begin 1 to 3 weeks after a person has been infected. Giardia infection rates have been known to go up in late summer.  Between 2006-2008 in the United States, known cases of giardiasis were twice as high between June-October as they were between January-March.   Anyone may become infected with Giardia. However, those at  greatest risk are :

    • Travelers to countries where giardiasis  is common
    • People  in child care settings
    • Those who are in close contact with  someone who has the disease
    • People who swallow contaminated drinking  water
    • Backpackers or campers who drink untreated water from lakes or rivers
    • People who have contact with animals who  have the disease
    • Men who have sex with men

     

    BIOLOGY

    Causal Agent:

    Giardia intestinalis is a protozoan flagellate (Diplomonadida). This protozoan was initially named Cercomonas intestinalis by Lambl in 1859.  It was renamed Giardia lamblia by Stiles in 1915 in honor of Professor A. Giard of Paris and Dr. F. Lambl of Prague. However, many consider the name, Giardia intestinalis, to be the correct name for this protozoan. The International Commission on Zoological Nomenclature is reviewing this issue.

     

    Life Cycle:

    Life Cycle of Giardia lamblia

    Cysts are resistant  forms and are responsible for transmission of giardiasis. Both cysts and trophozoites can be found in the feces (diagnostic stages). The cysts are hardy and can survive several months in cold water. Infection occurs by the ingestion of cysts in contaminated water, food,   or by the fecal-oral route (hands or fomites). In the small intestine, excystation releases trophozoites (each cyst produces two trophozoites). Trophozoites multiply by longitudinal binary fission,  remaining in the lumen of the proximal small bowel where they can be free or   attached to the mucosa by a ventral sucking disk. Encystation occurs as the parasites transit toward the   colon. The cyst is the stage found most commonly in nondiarrheal feces. Because the cysts are infectious when passed in the stool   or shortly afterward, person-to-person transmission is possible. While animals are infected with Giardia, their importance as a reservoir is unclear.

    Life cycle image and information courtesy of DPDx.

     

    DISEASE

    Giardiasis is the most frequently diagnosed intestinal parasitic disease in the United States and among travelers with chronic diarrhea. Signs and symptoms may vary and can last  for 1 to 2 weeks or longer. In some cases, people infected with Giardia have no symptoms.

    • Diarrhea
    • Gas
    • Greasy stools that tend to float
    • Stomach or abdominal cramps
    • Upset stomach or nausea/vomiting
    • Dehydration (loss of fluids)

    Other, less common symptoms include itchy skin, hives, and swelling of  the eye and join. Sometimes, the symptoms of giardiasis might seem to resolve, only to come back again after several days or weeks. Giardiasis can cause  weight loss and failure to absorb fat, lactose, vitamin A and vitamin B12.

    In children, severe giardiasis might delay physical and mental growth, slow development, and cause malnutrition.

     

    DIAGNOSIS

    Because Giardia cysts can be excreted intermittently, multiple stool collections (i.e., three  stool specimens collected on separate days) increase test. The  use of concentration methods and trichrome staining might not be sufficient to  identify Giardia because variability  in the concentration of organisms in the stool can make this infection  difficult to diagnose. For this reason, fecal immunoassays that are more  sensitive and specific should be used.

    Rapid immune-chromatographic cartridge assays  also are available but should not take the place of routine ova and parasite  examination. Only molecular testing (e.g., polymerase chain reaction) can  be used to identify the subtypes of Giardia.

     

    PREVENTION AND CONTROL

    • Practice good hygiene

    • Wash hands with soap and clean, running water for at least 20 seconds; rub your hands together to make a lather and be sure to scrub the backs of your hands, between your fingers, and under your nails.

    • Before, during, and after preparing food

    • Before eating food

    • Before and after caring for someone who is sick

    • Before and after treating a cut or wound

    • After using the toilet

    • After changing diapers or cleaning up a child who has used the toilet

    • After blowing your nose, coughing, or sneezing

    • After touching an animal or animal waste

    • After handling pet food or pet treats

    • After touching garbage

    • Help young  children and other people you are caring for with handwashing as needed

    • At child care  facilities

    • To reduce the  risk of spreading the disease, children with diarrhea should be removed from  child care settings until the diarrhea has stopped

    • At recreational  water venues (for example, pools, beaches, fountains)             

    • Protect others by  not swimming if you have diarrhea (this is most important for children in  diapers)

    • Shower before  entering the water

    • Wash children  thoroughly (especially their bottoms) with soap and water after they use the  bathroom or after their diapers are changed and before they enter the water

    • Take children on  frequent bathroom breaks and check their diapers often

    • Change diapers in  the bathroom, not by the water

    • Around animals             

    • Minimize contact  with the feces of all animals, especially young animals

    • When cleaning up  animal feces, wear disposable gloves and always wash hands when finished

    • Wash hands after  any contact with animals or their living areas

    • Thoroughly washing your hands after gardening can help prevent exposure to parasitic diseases.

    • Wash hands after gardening, even if wearing gloves

    • Avoid water (drinking and recreational) that may be contaminated

    • Do not swallow water while swimming in pools, hot tubs, interactive fountains, lakes, rivers, springs, ponds, streams or the ocean

    • Do not drink untreated water from lakes, rivers, springs, ponds, streams, or shallow wells

    • Do not drink poorly treated water or ice made from water during community outbreaks caused by contaminated drinking water

    • Do not use or  drink poorly treated water or use ice when traveling in countries where the  water supply might be unsafe

    • If the safety of  drinking water is in doubt (for example, during or after an outbreak, in a place with poor sanitation or lack of water treatment systems), do one of the following:

    • Drink bottled  water

    • Disinfect tap water by heating it to a rolling boil for 1 minute

    • Use a filter that has been tested and rated by National Safety Foundation (NSF) Standard 53 or NSF Standard 58 for cyst and oocyst reduction; filtered tap water will need additional treatment to kill or weaken bacteria and viruses

    • Avoid eating food that may be  contaminated

    • Use safe,  uncontaminated water to wash all food that is to be eaten raw

    • After washing  vegetables and fruit in safe, uncontaminated water, peel them if you plan to  eat them raw

    • Avoid eating raw or uncooked foods when traveling in countries with poor food and water treatment

    • Prevent contact and contamination with feces during sex

    • Use a barrier  during oral-anal sex

    • Wash hands right  after handling a condom used during anal sex and after touching the anus or  rectal area

    For more information view the source:Center for Disease Control

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  • HYMENOLEPIS NANA

    Hymenolepis infection or infection with the dwarf tapeworm is found worldwide. It is most often seen in children in countries in which sanitation and hygiene are inadequate. Although the dwarf  tapeworm infection rarely causes symptoms, it can be misdiagnosed for pinworm  infection.

     

    FAQs

    What  is Hymenolepis nana infection?

    The dwarf tapeworm  or Hymenolepis nana is found worldwide. Infection is most  common in children, in persons living in institutional settings, and in  people who live in areas where sanitation and personal hygiene is inadequate.

    How did I get infected?

    One becomes infected by accidentally ingesting dwarf tapeworm eggs. This can happen by ingesting fecally contaminated foods or water, by touching your mouth with contaminated fingers, or by ingesting contaminated soil. People can also become infected if they accidentally ingest an infected arthropod (intermediate host, such as a small beetle or mealworm) that has gotten into food.

    Adult dwarf tapeworms are very small in comparison with other tapeworms and may reach 15-40  mm (up to 2 inches) in length. The adult dwarf tapeworm is made up of many small segments, called proglottids As the dwarf tapeworm matures inside the intestine,  these segments break off and pass into the stool. An adult dwarf tapeworm can live for 4-6 weeks. However, once you are infected, the dwarf tapeworm may reproduce inside the body (autoinfection) and continue the infection.

    What are the symptoms of a dwarf tapeworm infection?

    Most people who are  infected do not have any symptoms. Those who have symptoms may experience  nausea, weakness, loss of appetite, diarrhea, and abdominal pain. Young  children, especially those with a heavy infection, may develop a headache,  itchy bottom, or have difficulty sleeping. Sometimes infection is misdiagnosed  as a pinworm infection.

    Contrary to popular  belief, a dwarf tapeworm infection does not generally cause weight loss. You cannot  feel the dwarf tapeworm inside your body.

    How is dwarf tapeworm infection diagnosed?

    Diagnosis is made by identifying dwarf tapeworm eggs in stool. Your health care provider will ask you to submit stool specimens collected over several days to see if you are infected.

    Is a dwarf tapeworm infection serious?

    No. Infection with the dwarf tapeworm is generally not serious. However, prolonged infection can lead to more severe symptoms; therefore, medical attention is needed to eliminate the dwarf tapeworm.

    How is a dwarf tapeworm infection treated?

    Treatment is available. A prescription drug called praziquantel is given. The medication causes the dwarf tapeworm to dissolve within the intestine. Praziquantel is generally well tolerated. Sometimes more than one treatment is necessary.

    Can infection be spread to other family members?

    Yes. Eggs are infectious (meaning they can re-infect you or infect others) immediately after being shed in feces.

    What should I do if I think I have a dwarf tapeworm infection?

    See your health care provider for diagnosis and treatment.

    How can dwarf tapeworm infection be prevented?

    To reduce the likelihood of infection you should:

    • Wash your hands with soap and warm water after using the toilet, changing diapers, and before preparing foods.
    • Teach children the importance of washing hands to prevent infection.
    • When traveling in countries where food is likely to be contaminated, wash, peel or cook all raw vegetables and fruits with safe water before eating.

     

    BIOLOGY

    Causal Agent

    Hymenolepiasis is primarily caused by the cestode (tapeworm) species, Hymenolepis nana (the dwarf tapeworm, adults measuring 15 to 40 mm in length).

     

    Life Cycle:

     

    Proposed life cycle of Hymenolepis nana

    Eggs of Hymenolepis   nana are immediately infective when passed with the stool and cannot survive   more than 10 days in the external environment. When eggs are ingested by an arthropod intermediate host  (various species of beetles and fleas may serve as intermediate   hosts), they develop into cysticercoids, which can infect humans or rodents upon ingestion and develop into adults in the small intestine. A morphologically   identical variant, H. nana var. fraterna, infects rodents and uses   arthropods as intermediate hosts. When eggs are ingested  (in contaminated food or water or from hands contaminated with   feces), the oncospheres contained in the eggs are released. The oncospheres   (hexacanth larvae) penetrate the intestinal villus and develop into cysticercoid larvae. Upon rupture of the villus, the cysticercoids return to   the intestinal lumen, evaginate their scoleces, attach to the intestinal mucosa and develop into adults   that reside in the ileal portion of the small intestine producing gravid  proglottids . Eggs are passed in the stool when released from   proglottids through its genital atrium or when proglottids disintegrate in the   small intestine. An alternate mode of infection consists of internal   autoinfection, where the eggs release their hexacanth embryo, which penetrates   the villus continuing the infective cycle without passage through the external environment. The life span of adult worms is 4 to 6 weeks, but internal autoinfection allows the infection to persist for years.

    Life cycle image and information courtesy of DPDx.

    For more information view the source:Center for Disease Control

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  • NEMATODES

    The nematodes or roundworms are the most diverse phylum of pseudocoelomates, and one of the most diverse of all animals. Nematode species are very difficult to distinguish; over 28,000 have been described, of which over 16,000 are parasitic. It has been estimated that the total number of nematode species might be approximately 1,000,000. Unlike cnidarians or flatworms, roundworms have a digestive system that is like a tube with openings at both ends.

    For more information view the source:Wikipedia


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  • PARAGONIMIASIS PARAGONIMUS WESTERMANI

    FAQS

    What is Paragonimus?

    Paragonimus is a parasitic lung fluke (flat worm). Cases of  infection occur after a person eats raw or undercooked infected crab or  crayfish. Paragonimus infection also can be very serious if the fluke  travels to the central nervous system, where it can cause symptoms that mimic meningitis.

     

    Where is Paragonimus  found?

    Paragonimus westermani and several  other species are found throughout eastern, southwestern, and southeast Asia;  (including China, the Philippines, Japan, Vietnam, South Korea, Taiwan, and  Thailand). P. africanus is found  in Africa, and P. mexicanus in Central and South America. P.  kellicotti is found in the mid-western and southern United States living in  crayfish. Some cases of infection have been associated with eating raw crayfish  on river raft trips in the Midwest. P. kellicotti or other species have  caused paragonimiasis after ingestion of raw freshwater crabs in sushi. There  are several species of Paragonimus in  other parts of the world that can infect humans.

     

    How is Paragonimus  transmitted?

    The infection is transmitted by eating crab or crawfish that is either, raw, partially cooked, pickled, or salted. The larval stages of the parasite  are released when the crab or crawfish is digested. They then migrate within  the body, ending up in the lungs. In 6-10 weeks the larvae mature into adult  flukes.

     

    What are the signs and symptoms?

    Adult flukes living in the lung cause lung  disease that may never be diagnosed or is thought to be tuberculosis. After 2-15 days, the initial signs and symptoms may be  diarrhea and abdominal pain. This may be followed several days later by fever, chest pain, and fatigue. The symptoms may also  include a dry cough initially, which later often becomes productive with  rusty-colored or blood-tinged sputum on exertion.

     

    How is Paragonimus infection diagnosed?

    The diagnosis is usually made by identifying Paragonimus eggs in the sputum or  sometime in the stool (from ingesting after coughing up).

     

    Is Paragonimus infection contagious?

    No. Paragonimus is not contagious.

     

    Is there treatment?

    Yes, there is treatment. Several drugs are available through  your physician after being accurately diagnosed.

     

    How can I prevent  Paragonimus infection?

    Never eat raw freshwater crabs or crayfish. Cook crabs and crayfish for to at least 145°F (~63°C). Travelers should be advised to avoid traditional meals containing undercooked freshwater crustaceans.

     

    EPIDEMIOLOGY & RISK FACTORS

    Several species of Paragonimus cause most infections; the most important is P.  westermani, which occurs primarily in Asia including China, the  Philippines, Japan, Vietnam, South Korea, Taiwan, and Thailand. P. africanus causes infection  in Africa, and P. mexicanus in Central and South America. Specialty dishes in which shellfish are consumed  raw or prepared only in vinegar, brine, or wine without cooking play a key role  in the transmission of paragonimiasis. Raw crabs or crayfish are also used in  traditional medicine practices in Korea, Japan, and some parts of Africa.

    Although rare, human paragonimiasis from P.  kellicotti has been acquired in the United States, with multiple  cases from the Midwest. Several cases have been associated with ingestion of  uncooked crawfish during river raft float trips in Missouri.

     

    BIOLOGY

    Causal Agent:

    More than 30 species of trematodes (flukes) of the genus Paragonimus have been reported which infect animals and humans. Among the more than 10 species reported to infect humans, the most common is P. westermani, the oriental lung fluke.

     

    Life Cycle:

    Life cycle of Paragonimus westermani

    The eggs are excreted unembryonated in the sputum, or alternately they are swallowed and passed with stool.   In the external environment, the eggs become embryonated, and  miracidia hatch and seek the first intermediate host, a snail, and penetrate its soft tissues.   Miracidia go through several developmental stages inside the snail: sporocysts,   rediae, with the latter giving rise to many   cercariae , which  emerge from the snail. The cercariae invade the second intermediate host, a crustacean such as a crab or   crayfish, where they encyst and become metacercariae. This is the infective stage for the mammalian   host.   Human infection with P. westermani occurs by eating inadequately cooked or pickled crab or crayfish that  harbor metacercariae of the parasite.   The metacercariae excyst in the duodenum, penetrate through the  intestinal wall into the peritoneal cavity, then through the abdominal wall and diaphragm into the lungs,   where they become encapsulated and develop into adults. The worms can also    reach other organs and tissues, such as the brain and striated muscles, respectively. However, when this   takes place completion of the life cycles is not achieved, because the eggs laid cannot exit these sites.   Time from infection to oviposition is 65 to 90 days. 

    Infections may persist for 20 years in humans. Animals such as pigs,  dogs, and a variety of feline species can also harbor P. westermani.

    Life cycle image and information courtesy of DPDx.

     

    DISEASE

    Paragonimiasis is an acute infection with cough, abdominal pain, discomfort, and low-grade fever that may occur 2 to15 days after infection. The infection usually resolves without treatment. Persons with light infections may have no symptoms. Symptoms of long-term infection may mimic bronchitis or tuberculosis, with coughing up of blood-tinged sputum.

     

    DIAGNOSIS

    The infection is usually diagnosed by identification of Paragonimus eggs in sputum. The eggs are sometimes found in stool samples (coughed-up eggs are swallowed). A tissue biopsy is sometimes performed to look for eggs in a tissue specimen.

    Specific and sensitive antibody tests based on P. westermani antigens are available through CDC, and serologic tests using a variety of techniques are available through commercial laboratories.

     

    PREVENTION AND CONTROL

    Never eat raw freshwater crabs or crayfish. Cook crabs and crayfish for to at least 145°F (~63°C). Travelers should be advised to avoid traditional meals containing undercooked freshwater crustaceans.

    For more information view the source:Center for Disease Control

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  • PROTOZOA

    Protozoa (from the Greek words proto, meaning first, and zoa, meaning animals; singular protozoon or also protozoan) are a diverse group of single-cell eukaryotic organisms, many of which are motile. Throughout history, protozoa have been defined as single-cell protists with animal-like behavior, e.g., movement. Protozoa were regarded as the partner group of protists to protophyta, which have plant-like behaviour, e.g., photosynthesis. The most important protozoans range usually from 10 to 52 micrometers, but can grow as large as 1 mm, and are seen easily by microscope.

    CHARACTERISTICS

    Protozoa commonly range from 10 to 52 micrometers, but can grow as large as 1 mm, and are seen easily by microscope. The largest protozoa known are the deep-sea dwelling xenophyophores, which can grow up to 20 cm in diameter. They were considered formerly to be part of the protista family. Protozoa exist throughout aqueous environments and soil, occupying a range of trophic levels.

    MOTILITY AND DIGESTION

    Tulodens are one of the slow-moving form of protozoans. They move around with whip-like tails called flagella, hair-like structures called cilia, or foot-like structures called pseudopodia. Others do not move at all. Protozoa may absorb food via their cell membranes, some, e.g., amoebas, surround food and engulf it, and yet others have openings or "mouth pores" into which they sweep food. All protozoa digest their food in stomach-like compartments called vacuoles.

    ECOLOGICAL ROLE

    As components of the micro- and meiofauna, protozoa are an important food source for microinvertebrates. Thus, the ecological role of protozoa in the transfer of bacterial and algal production to successive trophic levels is important. As predators, they prey upon unicellular or filamentous algae, bacteria, and microfungi. Protozoa are both herbivores and consumersin the decomposer link of the food chain. They also control bacteria populations and biomass to some extent. Protozoa such as the malaria parasites (Plasmodium spp.), trypanosomesand leishmania, are also important as parasites and symbionts of multicellular animals.

    LIFE CYCLE

    Some protozoa have life stages alternating between proliferative stages (e.g., trophozoites) and dormant cysts. As cysts, protozoa can survive harsh conditions, such as exposure to extreme temperatures or harmful chemicals, or long periods without access to nutrients, water, or oxygen for a period of time. Being a cyst enables parasitic species to survive outside of a host, and allows their transmission from one host to another. When protozoa are in the form of trophozoites (Greek, tropho = to nourish), they actively feed. The conversion of a trophozoite to cyst form is known as encystation, while the process of transforming back into a trophozoite is known as excystation.Protozoa can reproduce by binary fission or multiple fission. Some protozoa reproduce sexually, some asexually, while some use a combination, (e.g., Coccidia). An individual protozoon is hermaphroditic.

    CLASSIFICATION

    Protozoa were previously often grouped in the kingdom of Protista, together with the plant-like algae and fungus-like slime molds. As a result of 21st-century systematics, protozoa, along with ciliates, mastigophorans, and apicomplexans, are arranged as animal-like protists. With the possible exception of Myxozoa, protozoa are not categorized as Metazoa. Protozoa are unicellular organisms and are often called the animal-like protists because they subsist entirely on other organisms for food. Most protozoa can move about on their own. Amoebas, Paramecia, and Trypanosomes are all examples of animal-like Protists.

    HUMAN DISEASE

    Some protozoa are human parasites, causing diseases. Examples of human diseases caused by protozoa: Malaria Amoebiasis Giardiasis Toxoplasmosis Cryptosporidiosis Trichomoniasis Chagas disease Leishmaniasis Sleeping Sickness Dysentery

    For more information view the source:Wikipedia

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  • SCHISTOSOMA

    Schistosomiasis, also known as bilharzia, is  a disease caused by parasitic worms. Although the worms that cause schistosomiasis are not found in the United  States, more than 200 million people are infected worldwide. In terms of impact this disease is second only to malaria as the most devastating parasitic disease. Schistosomiasis  is considered one of the Neglected Tropical Diseases (NTDs).

    The parasites that  cause schistosomiasis live in certain types of freshwater snails. The  infectious form of the parasite, known as  cercariae, emerge from the snail, hence  contaminating water. You can become infected when your skin comes in contact  with contaminated freshwater. Most human  infections are caused by Schistosoma mansoni, S. haematobium, or S. japonicum.

     

    FAQS

    What is schistosomiasis?

    Schistosomiasis,  also known as bilharzia, is a disease caused by parasitic worms. Infection with Schistosoma mansoni, S. haematobium, and S. japonicum causes illness in humans; less commonly, S. mekongi and S. intercalatum can cause disease. Although the worms that cause schistosomiasis are not found in the United  States, more than 200 million people are infected worldwide.

     

    How can  I get schistosomiasis?

    Infection  occurs when your skin comes in contact with contaminated freshwater in which  certain types of snails that carry schistosomes are living.

    Freshwater becomes  contaminated by Schistosoma eggs when infected people urinate or defecate in the water. The eggs hatch, and  if certain types of freshwater snails are present in the water, the parasites develop  and multiply  inside the snails. The  parasite leaves the snail and enters the water where it can survive for about  48 hours. Schistosoma parasites can penetrate the skin of persons who are wading, swimming, bathing,  or washing in contaminated water. Within several weeks, parasite mature into  adult worms, residing in the blood  vessels of the body where the females produce eggs. Some of the eggs travel to  the bladder or intestine and are passed into the urine or stool.

     

    What are the signs and symptoms of schistosomiasis?

    Within  days after becoming infected, you may develop a rash or itchy skin. Fever,  chills, cough, and muscle aches can begin within 1-2 months of infection. Most  people have no symptoms at this early phase of infection.

    Eggs  travel to the intestine, liver or bladder, causing inflammation or scarring. Children who are repeatedly infected can develop anemia, malnutrition, and  learning difficulties. After years of infection, the parasite can also damage  the liver, intestine, lungs, and bladder. Rarely, eggs are found in the brain  or spinal cord and can cause seizures, paralysis, or spinal cord inflammation.

    Symptoms  of schistosomiasis are caused by the body's reaction to the eggs produced by  worms, not by the worms themselves.

     

    What should I do if I think I have schistosomiasis?

    See your health care provider. If you have traveled to countries where schistosomiasis is found and had contact with freshwater, describe in detail where and for how long you traveled. Explain that you may have been exposed to contaminated water.

     

    How is schistosomiasis diagnosed?

    Your health care provider may ask you to provide stool or urine samples to see if you have the parasite. A blood sample can also be tested for evidence of infection. For accurate results, you must wait 6-8 weeks after your last exposure to contaminated water before the blood sample is taken.

     

    What is the  treatment for schistosomiasis?

    Safe and  effective drugs are available for the treatment of schistosomiasis. You will be given pills to take for 1-2 days.

     

    Am I at  risk?

    If you live in or travel to areas where schistosomiasis occurs and your skin comes in contact with freshwater from canals, rivers, streams, ponds, or lakes, you are at risk of getting schistosomiasis.

     

    In  what areas of the world does schistosomiasis occur?

    • Africa: all freshwater in southern and sub-Saharan Africa–including the great lakes and rivers as well as smaller bodies of water–are at risk for schistosomiasis transmission. Transmission also occurs in the Mahgreb region of North Africa and the Nile River valley in Egypt and Sudan.
    • South America: Brazil, Suriname, Venezuela
    • Caribbean: Antigua, Dominican Republic, Guadeloupe, Martinique, Montserrat, Saint Lucia (risk is low)
    • The Middle East: Iran, Iraq, Saudi Arabia, Yemen
    • Southern China
    • Parts of Southeast Asia and the Philippines, Laos

     

    How  can I prevent schistosomiasis?

    • Avoid swimming or wading in freshwater when you are in countries in which schistosomiasis occurs. Swimming in the ocean and in chlorinated swimming pools is  safe.
    • Drink safe water. Although schistosomiasis is not transmitted by swallowing contaminated water, if your mouth or lips come in contact with water containing the parasites, you could become infected. Because water coming directly from canals, lakes, rivers, streams, or springs may be contaminated with a variety of infectious organisms, you should either boil water for 1 minute or filter water before drinking it. Boiling water for at least 1 minute will kill any harmful parasites, bacteria, or viruses present. Iodine treatment alone WILL NOT GUARANTEE that water is safe and free of all parasites.
    • Bath water should be heated for 5 minutes at 150°F. Water held in a storage tank for at least 48 hours should be safe for showering.
    • Vigorous towel drying after an accidental, very brief water exposure may help to prevent the Schistosoma parasite from penetrating the skin. You should NOT rely on vigorous towel drying to prevent schistosomiasis.

     

    EPIDEMIOLOGY & RISK FACTORS

    Schistosomiasis  is an important cause of disease in many parts of the world, most commonly in  places with poor sanitation. School-age children who live in these areas are  often most at risk because they tend to spend time swimming or bathing in water  containing infectious cercariae. If  you live in, or travel to, areas where schistosomiasis is found and are exposed  to contaminated freshwater, you are at risk. Areas  where human schistosomiasis is found include:

    Schistosoma  mansoni            

    • distributed throughout Africa: There is risk of infection in freshwater in southern and sub-Saharan Africa–including the great lakes and rivers as well as smaller bodies of water. Transmission also occurs in the Nile River valley in Sudan and Egypt
    • South America: including Brazil, Suriname, Venezuela
    • Caribbean (risk is low): Antigua, Dominican Republic, Guadeloupe, Martinique, Montserrat, and Saint Lucia.

    S. haematobium           

    • distributed throughout Africa: There is risk of infection in freshwater in southern and sub-Saharan Africa–including the great lakes and rivers as well as smaller bodies of water. Transmission also occurs in the Nile River valley in Egypt and the Mahgreb region of North Africa.
    • found in areas of the Middle East

     

    BIOLOGY

    Causal Agent:

    Schistosomiasis is caused by   digenetic blood trematodes. The three main species infecting humans are Schistosoma haematobium, S. japonicum, and S. mansoni. Two other species, more localized geographically, are S. mekongi and S. intercalatum. In addition, other species of schistosomes, which parasitize   birds and mammals, can cause cercarial dermatitis in humans.

     

    Life Cycle:

     

    Life Cycle of Schistomes

    Eggs are eliminated with feces or urine. Under optimal conditions the eggs hatch and release miracidia , which swim and penetrate specific snail intermediate hosts. The stages in the snail include 2 generations of sporocysts and the production of cercariae. Upon release from the snail, the infective cercariae swim, penetrate   the skin of the human host, and shed their forked tail, becoming schistosomulae. The schistosomulae migrate through several tissues and stages to   their residence in the veins. Adult worms in humans reside in the mesenteric venules in various   locations, which at times seem to be specific for each species. For instance, S. japonicum is more frequently found   in the superior mesenteric veins draining the small intestine, and S. mansoni occurs more often in the superior   mesenteric veins draining the large intestine. However, both species can occupy either location, and they   are capable of moving between sites, so it is not possible to state   unequivocally that one species only occurs in one location. S. haematobium most often occurs in the venous plexus of bladder, but it can also be found in the rectal venules. The females   (size 7 to 20 mm; males slightly smaller) deposit eggs in the small venules of   the  portal and perivesical systems. The eggs are moved progressively toward   the lumen of the intestine (S. mansoni and S. japonicum) and of   the bladder and ureters (S. haematobium), and are eliminated with feces   or urine, respectively.  Pathology of S. mansoni and S. japonicum schistosomiasis includes: Katayama fever, hepatic perisinusoidal egg granulomas,   Symmers’ pipe stem periportal fibrosis, portal hypertension, and occasional   embolic egg granulomas in brain or spinal cord. Pathology of S. haematobium schistosomiasis includes: hematuria, scarring, calcification,   squamous cell carcinoma, and occasional embolic egg granulomas in brain or   spinal cord.

    Human contact with water   is thus necessary for infection by schistosomes. Various animals, such as dogs,   cats, rodents, pigs, hourse and goats, serve as reservoirs for S. japonicum, and dogs for S. mekongi.

    Life cycle image and information courtesy of DPDx.

     

    DISEASE

    Infection occurs  when skin comes in contact with contaminated freshwater in which certain types  of snails that carry the parasite are living. Freshwater becomes contaminated  by Schistosoma eggs when infected people urinate or defecate in the water. The eggs hatch, and  if  the appropriate species of snails are  present in the water, the parasites infect, develop and multiply inside the  snails. The parasite leaves the snail and enters the water where it can survive  for about 48 hours. Schistosoma parasites can penetrate the skin of persons who come in contact with  contaminated freshwater, typically when wading, swimming, bathing, or washing. Over several weeks, the parasites migrate  through host tissue and develop into adult worms  inside the blood vessels of the body. Once  mature, the worms mate and females produce eggs. Some of these eggs travel to  the bladder or intestine and are passed into the urine or stool.

    Symptoms of  schistosomiasis are caused not by the worms themselves but by the body’s  reaction to the eggs. Eggs shed by the adult worms that do not pass out of the  body can become lodged in the intestine or bladder, causing inflammation or  scarring. Children  who are repeatedly  infected can develop anemia, malnutrition, and learning difficulties. After  years of infection, the parasite can also damage the liver, intestine, spleen, lungs,  and bladder.

     

    Common Symptoms

    Most  people have no symptoms when they are first infected. However, within days after becoming infected, they may develop  a rash or itchy skin. Within 1-2 months of infection, symptoms may develop  including fever, chills, cough, and muscle aches.

     

    Chronic  schistosomiasis

    Without  treatment, schistosomiasis can persist for years. Symptoms of chronic  schistosomiasis include: abdominal pain, enlarged liver, blood in the stool or  blood in the urine, problems passing urine, and increased risk of bladder  cancer.

    Rarely,  eggs are found in the brain or spinal cord and can cause seizures, paralysis,  or spinal cord inflammation.

     

    DIAGNOSIS

    Stool  samples can be examined microscopically for parasite eggs (S. mansoni or S. japonicum) or urine (S. haematobium). The eggs tend to be passed intermittently and in  small amounts and may not be detected, so it may be necessary to perform a  blood (serologic) test.

     

    PREVENTION AND CONTROL

    No vaccine is available. The best way to prevent schistosomiasis is to take the following steps if you are visiting or live in an area where schistosomiasis is transmitted:

    • Avoid swimming or wading in freshwater when you are in countries in which schistosomiasis occurs. Swimming in the ocean and in chlorinated swimming pools is safe.
    • Drink safe water. Although schistosomiasis is not transmitted by swallowing contaminated water, if your mouth or lips come in contact with water containing the parasites, you could become infected. Because  water coming directly from canals, lakes, rivers, streams, or springs may be contaminated with a variety of infectious organisms, you should either bring your water to a rolling boil for 1 minute or filter water before drinking it. Bring your water to a rolling boil for at least 1 minute will kill any harmful parasites, bacteria, or viruses present. Iodine treatment alone WILL NOT GUARANTEE that water is safe and free of all parasites.
    • Water used for bathing should be brought to a rolling boil for 1 minute to kill any cercariae, and then cooled before bathing to avoid scalding. Water held in a storage tank for at least 1 - 2 days should be safe for bathing.
    • Vigorous towel drying after an accidental, very brief water exposure may help to prevent the Schistosoma parasite from penetrating the skin. However, do not rely on vigorous towel drying alone to prevent schistosomiasis.

    Those who have had contact with potentially contaminated water overseas should see their health care provider after returning from travel to discuss testing.

    For more information view the source:Center for Disease Control

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  • STRONGYLOIDES STERCORALIS

    Strongyloidiasis was first described in French troops stationed in modern day Vietnam during the late 19th century who were suffering from severe, persistent diarrhea. It is a parasitic disease caused by nematodes, or roundworms, in the genus Strongyloides that enter the body through exposed skin, such as bare feet.  Strongyloides is most common in tropical or subtropical climates.

    Most people who are infected with Strongyloides do not know they are infected and have no symptoms. Others may develop a severe form and, if untreated, become critically ill and potentially die.

     

    FAQS

    What is strongyloidiasis?

    Strongyloidiasis  is a disease caused by a nematode, or a roundworm, in the genus Strongyloides. Though there are over 40  species within this genus that can infect birds, reptiles, amphibians, livestock  and other primates, Strongyloides  stercoralis is the primary species that accounts for human disease. The  larvae are small; the longest reach about 1.5mm in length -- the size of a  mustard seed or a large grain of sand.

    How do people get infected with strongyloides?

    Strongyloides is classified as a soil-transmitted helminth. This means that the primary mode of infection is through contact with soil that is contaminated with free-living larvae. When the larvae come in contact with skin, they are able to penetrate it and migrate through the body, eventually finding their way to the small intestine where they burrow and lay their eggs. Unlike other soil-transmitted helminths such as hookworm and whipworm whose eggs do not hatch until they are in the environment, the eggs of Strongyloides hatch into larvae in the intestine. Most of these larvae will be excreted in the stool, but some of the larvae may molt and immediately re-infect the host either by burrowing into the intestinal wall, or by penetrating the perianal skin. This characteristic of Strongyloides is termed auto-infection. The significance of auto-infection is that unless treated for Strongyloides, persons may remain infected throughout their lifetime. In addition to contact with soil and auto-infection, there have been rare cases of person-to-person transmission in:

    • organ transplantation
    • institutions for the developmentally disabled
    • daycare centers.

    Where do most cases of strongyloidiasis occur in the United States?

    In the United States, Strongyloides has classically been associated with uniformed-service veterans who returned from  tropical regions such as Southeast Asia and the South Pacific during World War  II. Small domestic studies have shown locations of infection in rural  Appalachia. The highest rates in the United States have been documented in  immigrant populations.

    Strongyloides is more commonly found in areas that are  relatively warm and moist, in rural areas, and areas associated with  agricultural activity, but it can occur anywhere. It is found more frequently  in socio-economically disadvantaged persons and in institutionalized  populations.

    What are the signs and symptoms of strongyloidiasis?

    The majority of people infected with Strongyloidesare without symptoms. Those who do develop symptoms  tend to have non-specific, or generalized complaints. Some people develop  abdominal pain, bloating, heartburn, intermittent episodes of diarrhea and  constipation, a dry cough, and rashes. Rarely people will develop arthritis,  kidney problems, and heart conditions. Strongyloidiasis can be severe and life-threatening in  persons who:

    • are on oral or intravenous steroids -- such as those  with asthma or chronic obstructive pulmonary disease (COPD) exacerbations, lupus,  gout,  or in persons using steroids for  immunosuppression or symptomatic relief
    • are infected with the virus HTLV-1
    • have hematologic malignancies such as leukemia  or lymphoma
    • are  transplant recipients.

    How soon after the exposure do symptoms develop?

    Most people do not know when their exposure occurred.  For those who do, a local rash can occur immediately. The cough usually occurs several days later. Abdominal symptoms typically occur approximately 2 weeks later, and larvae can be found in the stool about 3 to 4 weeks later.

    What should I do if I think I might have strongyloidiasis?

    See your health care provider.

    How is infection with Strongyloides diagnosed?

    Strongyloides is  classically diagnosed by visualization of larvae on microscopic stool examination.  This may require that you provide multiple stool samples to your doctor or the  laboratory. Some laboratories are capable of diagnosing Strongyloides with blood tests.

    How is strongyloidiasis treated?

    Safe and effective drugs are available to treat infection with Strongyloides.

    How can strongyloidiasis be prevented?

    The best way to prevent Strongyloides infection is to wear shoes when you are walking on soil, and to avoid contact with fecal matter or sewage. Proper sewage disposal and fecal management are keys to prevention.

     

    EPIDEMIOLOGY & RISK FACTORS

    Strongyloides is  known to exist on all continents except for Antarctica, but it is most common  in the tropics, subtropics, and in warm temperate regions. The global prevalence of Strongyloides is unknown, but experts estimate that there are  between 3 – 100 million infected persons worldwide.

    In the United States, a series of small studies in select populations have shown that between 0-6.1% of persons sampled were infected. Studies in immigrant populations have shown a  much higher percentage of infected persons ranging from 0-46.1%.

    Strongyloides is  found more frequently in the socioeconomically disadvantaged, in institutionalized  populations, and in rural areas. It is often associated with agricultural  activities.

    The most common way of becoming infected with Strongyloides is by contacting soil that  is contaminated with Strongyloides larvae. Therefore, activities that increase contact with the soil increase the  risk of becoming infected, such as:

    • walking with bare feet
    • contact with human waste or sewage
    • occupations that increase contact with  contaminated soil such as farming and coal mining.

    Furthermore, many studies have shown an association with Strongyloides and infection with Human  T-Cell Lymphotropic Virus-1 (HTLV-1). These studies have shown that people infected  with HTLV-1 are more likely to become infected with Strongyloides, and that once infected, are more likely to develop  severe cases of strongyloidiasis.

    Of note, being infected with HIV/AIDS has not been shown to  be a risk factor for developing Strongyloides or having a worse clinical course.

     

    BIOLOGY

    Causal Agent:

    The nematode (roundworm) Strongyloides stercoralis.  Other Strongyloides include S. fülleborni, which infects chimpanzees and baboons and may produce limited infections in humans.

     

    Life Cycle:

     

    Life Cycle of Strongyloides

    The Strongyloides life cycle is more complex than that of most nematodes with its alternation between free-living and parasitic cycles, and its potential for autoinfection and multiplication within the host. Two types of cycles exist:

    Free-living cycle: The rhabditiform larvae passed in the stool  can either molt twice and become infective filariform larvae (direct development) or molt four times and become free living adult males and females  that mate and produce eggs  from which rhabditiform larvae hatch. The latter in turn can either develop into a new generation of free-living adults or into infective filariform larvae. The filariform larvae penetrate the human host skin to initiate the parasitic cycle.

    Parasitic cycle: Filariform larvae in contaminated soil penetrate the human skin, and are transported to the lungs where they penetrate the alveolar spaces; they are carried through the bronchial tree to the pharynx, are swallowed and then reach the small intestine. In the small intestine they molt twice and become adult female worms. The females live threaded in the epithelium of the small intestine and by parthenogenesis produce eggs, which yield rhabditiform larvae. The rhabditiform larvae can either be passed in the stool. In autoinfection, the rhabditiform larvae become infective filariform larvae, which can penetrate either the intestinal mucosa (internal autoinfection) or the skin of the perianal area (external autoinfection); in either case, the filariform larvae may follow the previously described route, being carried successively to the lungs, the bronchial tree, the pharynx, and the small intestine where they mature into adults; or they may disseminate widely in the body. To date, occurrence of autoinfection in humans with helminthic infections is recognized only in Strongyloides stercoralis and Capillaria philippinensis infections. In the case of Strongyloides, autoinfection may explain the possibility of persistent infections for many years in persons who have not been in an endemic area and of hyperinfections in immunodepressed individuals.

    Life cycle image and information courtesy of DPDx.

     

    DISEASE

    Most people infected with Strongyloidesdo not know they’re infected. If they do feel sick the most common  complaints are the following. Abdominal:   

    • stomachache, bloating, and heartburn
    • intermittent episodes of diarrhea and constipation
    • nausea and loss of appetite

    Respiratory:  

    • dry cough
    • throat irritation

    Skin:  

    • an itchy, red rash that occurs where the worm entered the skin
    • recurrent raised red rash typically along the thighs and buttocks.

    Rarely, severe life-threatening forms of the disease called hyperinfection syndrome and  disseminated strongyloidiasis can occur. These forms of the disease are more common in people who are on corticosteroids (prednisone for example) or other immunosuppressive therapies or who are infected with HTLV-1. In this situation, people become critically ill, and should be taken to the hospital immediately.

     

    DIAGNOSIS

    Strongyloides is usually  diagnosed by seeing  larvae in stool when  examined under the microscope. This may require that you provide multiple stool  samples to your doctor or the laboratory. Some laboratories are capable of  diagnosing Strongyloides with blood  tests.

     

    PREVENTION AND CONTROL

    The best way to prevent Strongyloidesinfection is to wear shoes when you are walking on soil, and to avoid contact  with fecal matter or sewage. Proper sewage disposal and fecal management are  keys to prevention.  Furthermore, if you believe that you may be infected, the  best way to prevent severe disease is to be tested and, if found to be positive  for disease, treated.  You should discuss testing with your doctor if you are:

    • taking  steroids or other immunosuppressive therapies
    • about to start taking steroids or other  immunosuppressive therapies
    • a veteran who served in the South Pacific or  southeast Asia
    • infected with Human T-cell Lymphotropic Virus-1  (HTLV-1)
    • diagnosed with cancer
    • going to donate or receive organ transplants.

    For more information view the source:Center for Disease Control

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  • TAENIA SOLIUM

    Taenia solium, also called the pork tapeworm, is a cyclophyllid cestode in the family Taeniidae. It infects pigs and humans in Asia, Africa, South America, parts of Southern Europe and pockets of North America. In the larval stage, it causes cysticercosis which is a major cause of seizures in humans. Like all cyclophyllid cestodes, T. solium has four suckers on its scolex ("head"). T. solium also has two rows of hooks.

     

    DESCRIPTION

    T. solium is normally 2 m to 3 m in length, but can become very large, over 50 m long in some situations. T. solium has a very similar life cycle to Taenia saginata. Cysticerci have three morphologically distinct types. The common one is the ordinary "cellulose" cysticercus which has a fluid filled bladder that is 0.5 cm to 1.5 cm in length and an invaginated scolex. The intermediate form has a scolex while the "racemose" has no evident scolex but are believed to be larger and much more dangerous. They are 20 cm in length and have 60 ml of fluid and 13% of patients might have all three types in the brain. Humans are usually infected through eating infected pork, fostering adult tapeworms in the intestine, and passing eggs through feces, but autoinfection is also possible. In that case, a cysticercus (a larva sometimes called a "bladder worm") develops in the human and the human acts like an intermediate host. This happens if eggs get to the stomach, usually as a result of contaminated hands, but also due to retroperistalsis. Cysticerci often occur in the central nervous system, which can cause major neurological problems like hydrocephalus, paraplegy, meningitis, convulsions and even death. The condition of having cysticerci in one's body is called cysticercosis. Eggs can be diagnosed only to the family level, but if a proglottid's uterus is stained with India ink, the number of visible uterine branches can help identify the species: unlike the Taenia saginata uteri, T. solium uteri have only five to ten uterine branches on each side. Infection with T. solium adults is treated with niclosamide, which is one of the most popular drugs for adult tapeworm infections, as well as for fluke infections. As cysticercosis is a major risk, it is important to wash one's hands before eating and to suppress vomiting if a patient may be infected with T. solium. If neurocysticercosis occurs the drug of choice is either albendazole or praziquantel. These drugs damage the parasites skin internally causing it to disintegrate and is then removed by the host's immune system. Infection may be prevented with proper disposal of human feces around pigs, cooking meat thoroughly and/or freezing the meat at -10 ?C for 5 days. Most cases occur because infected food handlers contaminate the food.

    PATHOGENESIS

    Ingestion of T. solium eggs or proglottid rupture within the host intestine can cause larvae to migrate into host tissue and cause cysticercosis. This is the most frequent and severe disease caused by T. solium. In symptomatic cases, a wide spectrum of symptoms may be expressed including headaches, dizziness and occasional seizures. In more severe cases, dementia or hypertension due to perturbation of the normal circulation of cerebrospinal fluid can occur. The severity of cysticercosis depends on location, size and number of parasite larvae in tissues, as well as the host immune response. Other symptoms include sensory deficits, involuntary movements and brain system dysfunction. In children ocular location of cysts is more common than cystation in other locations of the body. If a person is heavily infected with T. solium, it can lead to neurocysticercosis which can lead to epilepsy, seizures, lesions in the brain, blindness and tumor like growths. This kind of patient will also show the low level of eosinophils when they run the blood test.

    DIAGNOSIS

    Diagnosis requires biopsy of the infected tissue and examination of feces. T. solium eggs and proglottids found in feces diagnoses taeniasis and not cysticercosis. Cysticercosis is diagnosed primarily on confirming the presence of hooks on the scolex of T. solium. Radiological test such as X-ray, CT scans which demonstrate "ring-enhancing brain lesions", and MRIs can also be used to detect diseases. X-rays are used to identify calcified larvae in the subcutaneous and muscle tissues and CT scans and MRIs are used to find lesions in the brain.

    TREATMENT

    PZQ (praziquantel) is the drug of choice for the treatment of T. solium infection. Some consider Niclosamide to be the drug of choice for all types of Tapeworms. For cysticercosis, one can be treated with albendazole combining with steroid to reduce the inflammation. Surgical intervention may be necessary to treat CNS lesions. Albendazole appears to be more effective and a safe drug for Neurocysticercosis, infection of the brain with T. solium larvae.

    PREVENTION AND CONTROL

    The best way to avoid getting tapeworms is to not eat under-cooked pork. Moreover, a high level of personal hygiene and prevention of fecal contamination of pig foods also plays a major role in prevention of getting the parasites.

    EPIDEMIOLOGY

    T. solium is found worldwide, however, it has shown to be more common in cosmopolitan areas. Because pigs are intermediate hosts of the parasite, completion of the life cycle occurs in regions where humans live in close contact with pigs and eat undercooked pork. Cysticercosis is often seen in areas where poor hygiene allows for contamination of food, soil or water supplies. Prevalence rates in the United States have shown that immigrants from Mexico, Central and South America and South-east Asia account for most of the domestic cases of cysticercosis. Taeniasis and cysticercosis are very rare in predominantly Muslim countries, as Islam forbids the consumption of pork. It is important to note that human cysticercosis is acquired by ingesting T. solium eggs shed in the feces of a human tapeworm carrier via gravid proglottids, and thus can occur in populations that neither eat pork nor share environments with pigs, although, as stated, the completion of the life cycle can occur only where humans live in close contact with pigs and eat pork. In 1990 and 1991, four unrelated members of an Orthodox Jewish community in New York City developed recurrent seizures and brain lesions which were found to have been caused by cysticercosis from T. solium. In keeping with their religion, none of the patients ate pork; additionally, none had any history of recent foreign travel. Several immediate family members of these four patients with seizures were found to have cysticercus antibodies. The families of the four patients had all employed housekeepers from Latin American countries, and one of the housekeepers tested positive for cysticercus antibodies, leading to the conclusion that the housekeepers were the most likely source of the infections.

    LIFE CYCLE

    This infection is caused by ingestion of eggs shed in the feces of a human tapeworm carrier. Pigs and humans become infected by ingesting eggs or gravid proglottids. Humans are infected either by ingestion of food contaminated with feces containing eggs, or by autoinfection. In the latter case, a human infected with adult T. solium can ingest eggs produced by that tapeworm, either through fecal contamination or, possibly, from proglottids carried into the stomach by reverse peristalsis. Once eggs are ingested, oncospheres hatch in the intestine, invade the intestinal wall, and migrate to striated muscles, as well as the brain, liver, and other tissues, where they develop into cysticerci. In humans, cysts can cause serious sequelae if they localize in the brain, resulting in neurocysticercosis. The parasite life cycle is completed, resulting in human tapeworm infection, when humans ingest undercooked pork containing cysticerci. Cysts evaginate and attach to the small intestine by their scolex. Adult tapeworms develop, (up to 2 to 7 m in length and produce less than 1000 proglottids, each with approximately 50,000 eggs) and reside in the small intestine for years.

     

     

    For more information view the source:Wikipedia

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  • TAENIA SOLIUM SAGINATA

    Taeniasis  in humans is a parasitic infection caused by the tapeworm species Taenia saginata (beef tapeworm), Taenia solium (pork tapeworm), and Taenia asiatica (Asian tapeworm). Humans  can become infected with these tapeworms by eating raw or undercooked beef (T. saginata) or pork (T. solium and T. asiatica). People with taeniasis may not know they have a  tapeworm infection because symptoms are usually mild or nonexistent.

    Taenia solium tapeworm infections can lead to, which is a disease that can cause seizures, so it  is important seek treatment.

     

    FAQS

    What is taeniasis?

    Taeniasis  in humans is a parasitic infection caused by the tapeworm species Taenia saginata (beef tapeworm), Taenia solium (pork tapeworm), and Taenia asiatica (Asian tapeworm). Humans  can become infected with these tapeworms by eating raw or undercooked beef (T. saginata) or pork (T. solium and T. asiatica). People with taeniasis may not know they have a  tapeworm infection because symptoms are usually mild or nonexistent.

    T. solium tapeworm infections can lead to cysticercosis, which is a disease that can cause seizures, so it  is important seek treatment.

     

    Where does taeniasis occur?

    Taenia saginata and T. solium are found worldwide. Infections with T. saginata occur wherever contaminated raw beef is eaten,  particularly in Eastern Europe, Russia, eastern Africa and Latin America. Taeniasis due to T. saginata is rare  in the United States, except in places where cattle and people are concentrated  and sanitation is poor, such as around feed lots where cattle can be exposed to  human feces. Tapeworm infections due to T. solium are more prevalent in under-developed communities with poor  sanitation and where people eat raw or undercooked pork. Higher rates of illness have been seen in people  in Latin America, Eastern Europe, sub-Saharan Africa, India, and Asia. Taenia  solium taeniasis is seen in the United States, typically among Latin  American immigrants. Taenia asiatica is limited to Asia and is seen mostly in the Republic of Korea, China, Taiwan,  Indonesia, and Thailand.

     

    What are the signs and symptoms of taeniasis?

    Most  people with tapeworm infections have no symptoms or mild symptoms. Patients  with T. saginata taeniasis often experience more symptoms that those with T. solium  or T. asiatica infections because the T. saginata tapeworm is larger in size (up to 10 meters (m)) than the other  two tapeworms (usually 3 m). Tapeworms can cause digestive problems including  abdominal pain, loss of appetite, weight loss, and upset stomach. The most visible sign of taeniasis is the active passing of proglottids (tapeworm segments) through the anus and in the feces. In rare cases,  tapeworm segments become lodged in the appendix, or the bile and pancreatic  ducts.

    Infection  with T. solium tapeworms can result in human cysticercosis, which can be a very  serious disease that can cause seizures and muscle or eye damage.

    Taenia saginata does not cause cysticercosis in humans. It is not clear if T. asiatica causes cysticercosis in humans or not.

     

    Is taeniasis common?

    Taeniasis  is under-reported in a significant portion of the world because diagnosis is  difficult in resource-poor settings.  The  number of new cases in the U.S. each year is probably less than 1000, but an  exact number is not known.

     

    What should I do if I think I have taeniasis?

    Contact your health care provider for proper diagnosis and care.

     

    Is medication available to treat taeniasis?

    Yes. Praziquantel is the drug of choice. Niclosamide is an alternative drug. See your health care provider for proper diagnosis and care.

     

    How did I get taeniasis?

    Eating raw or undercooked contaminated beef or pork is the primary risk factor for acquiring taeniasis. Because of this, certain groups with dietary restrictions for these meats may have a lower risk of taeniasis.

     

    How can I prevent infection with taeniasis?

    One way to prevent taeniasis is to cook meat to safe temperatures. A food thermometer should be used to measure the internal temperature of cooked meat. Do not sample meat until it is cooked. USDA recommends the following for meat preparation.

    For Whole Cuts of Meat (excluding poultry)                    

    • Cook to at least 145° F (63° C) as measured with a food thermometer placed in the thickest part of the meat, then allow the meat to rest* for three minutes before carving or consuming.
    • According to USDA, "A 'rest time' is the amount of time the product remains at the final temperature, after it has been removed from a grill, oven, or other heat source. During the three minutes after meat is removed from the heat source, its temperature remains constant or continues to rise, which destroys pathogens."

     

    Should I be concerned about spreading taeniasis to the rest of my household?

    No. However, a disease called cysticercosis can occur when T. solium tapeworm eggs are ingested. For example, people with poor hygiene who have taeniasis -- with or without symptoms -- will shed tapeworm eggs in their feces and might accidentally contaminate their environment. This can lead to transmission of cysticercosis to themselves or others unknowingly.

     

    Can I get taeniasis from my dog or cat that was diagnosed with tapeworm infection?

    In general, no. The tapeworm that your pet  was diagnosed with is more than likely the flea tapeworm (Dipylidium caninum). Dog or cat tapeworm infections are a result of your  pet swallowing a parasite-contaminated flea. Only in very rare instances do humans accidentally  swallow the contaminated fleas.

     

    EPIDEMIOLOGY & RISK FACTORS

    The tapeworms that cause taeniasis (Taenia saginata, T. solium, and T. asiatica) are found worldwide. Eating raw or undercooked beef or pork is the primary risk factor for acquiring taeniasis. Persons who don't eat raw or undercooked beef or pork are not likely to get taeniasis.

    Infections with T. saginata occur wherever contaminated raw beef is eaten, particularly in Eastern Europe, Russia, eastern Africa and Latin America. Taeniasis due to T. saginata is rare in the  United States, except in places where cattle and people are concentrated and  sanitation is poor, such as around feed lots when cattle can be exposed to  human feces. Tapeworm infections due to T. solium are more prevalent in under-developed communities with poor  sanitation and where people eat raw or undercooked pork. Higher rates of illness have been seen in people  in Latin America, Eastern Europe, sub-Saharan Africa, India, and Asia. Taenia  solium taeniasis is seen in the United States, typically among Latin  American immigrants. Taenia asiatica is limited to Asia and is seen mostly in the Republic of Korea, China, Taiwan,  Indonesia, and Thailand.

    A disease called cysticercosis can occur when T. solium tapeworm eggs are ingested. For example, people with poor hygiene who have taeniasis -- with or without symptoms -- will shed tapeworm eggs in their feces and might accidentally contaminate their environment. This can lead to transmission of cysticercosis to themselves or others.

     

    BIOLOGY

    Causal Agent:

    The cestodes (tapeworms) Taenia saginata (beef tapeworm) and T. solium (pork tapeworm). Taenia solium eggs can also cause cysticercosis.

     

    Life Cycle:

    Life Cycle of  Taenia saginata and Taenia solium

    Taeniasis is the infection of humans with the adult tapeworm of Taenia saginata or Taenia solium. Humans are the only definitive hosts for T. saginata and T. solium. Eggs or gravid proglottids are passed with feces; the eggs can survive for days to months in the   environment. Cattle (T. saginata) and pigs (T. solium) become   infected by ingesting vegetation contaminated with eggs or gravid proglottids. In the animal's intestine, the oncospheres hatch, invade the intestinal wall, and migrate to the striated   muscles, where they develop into cysticerci. A cysticercus can survive for   several years in the animal. Humans become infected by ingesting raw or   undercooked infected meat. In the human intestine, the cysticercus develops over 2 months into   an adult tapeworm, which can survive for years. The adult tapeworms attach to the small intestine by their scolex and reside in the small intestine. Length of adult worms is usually 5 m or less for T.  saginata (however it may reach up to 25 m) and 2 to 7 m for T. solium. The adults produce proglottids which mature, become gravid, detach from the tapeworm, and migrate to the anus or are passed in the stool   (approximately 6 per day). T. saginata adults usually have 1,000 to   2,000 proglottids, while T. solium adults have an average of 1,000   proglottids. The eggs contained in the gravid proglottids are released after   the proglottids are passed with the feces. T. saginata may produce up to   100,000 and T. solium may produce 50,000 eggs per proglottid respectively.

    Life cycle image and information courtesy of DPDx.

     

    DISEASE

    Human taeniasis  is a parasitic infection caused by three tapeworm species, T. saginata (known as the beef tapeworm), T. solium (pork tapeworm), and T. asiatica (the Asian tapeworm). Humans are the only hosts for these Taenia tapeworms. Humans pass the tapeworm  segments and/or eggs in feces and contaminate the soil in areas where  sanitation is poor. Taenia eggs can  survive in a moist environment and remain infective for days to months. Cows and pigs become infected after feeding  in areas that are contaminated with Taenia eggs from human feces. Once inside the cow or pig, the Taenia eggs hatch in the animal’s intestine and migrate to striated  muscle to develop into cysticerci, causing a disease known as cysticercosis. Cysticerci can survive for several years in animal muscle. Humans become  infected with tapeworms when they eat raw or undercooked beef or pork containing  infective cysticerci. Once inside humans, Taenia cysticerci migrate to the small intestine and mature to adult tapeworms,  which produce segments and eggs that are passed in feces.

     

    Symptoms

    Most  people with tapeworm infections have no symptoms or mild symptoms. Patients  with T. saginata taeniasis often experience more symptoms that those with T. solium because the T. saginata tapeworm  is larger in size (up to 10 meters (m)) than  T. solium (usually 3 m). Tapeworms can cause digestive problems including  abdominal pain, loss of appetite, weight loss, and upset stomach. The most  visible symptom of taeniasis is the active passing of proglottids (tapeworm segments) through the  anus and in the feces. In rare cases, tapeworm segments become  lodged in the appendix, or the bile and pancreatic ducts.

    Infection  with T. solium tapeworms can result in human cysticercosis, which can be a very serious disease that can  cause seizures and muscle or eye damage.

    Taenia saginata does not cause cysticercosis in humans. It is not clear if T. asiatica causes cysticercosis in humans or not.

     

    DIAGNOSIS

    Diagnosis of Taenia tapeworm infections is made by examination of stool samples; individuals should also be asked if they have  passed tapeworm segments. Stool specimens should be collected on three different days and examined in the lab for Taenia eggs using a microscope. Tapeworm eggs can  be detected in the stool 2 to 3 months after the tapeworm infection is established.

    Tapeworm eggs of T. solium can also infect humans, causing cysticercosis. It is important to diagnose and treat all tapeworm infections.

     

    PREVENTION AND CONTROL

    One way to prevent taeniasis is to cook meat to safe temperatures. A food thermometershould be used to measure the internal temperature of cooked meat. Do not sample meat until it is cooked. USDA recommends the following for meat preparation.

    For Whole Cuts of Meat (excluding poultry)                    

    • Cook to at least 145° F (63° C) as measured with a food thermometer placed in the thickest part of the meat, then allow the meat to rest* for three minutes before carving or consuming.

    For Ground Meat (excluding poultry)

    • Cook to at least 160° F (71° C); ground meats do not require a rest* time.
    • *According to USDA, "A 'rest time' is the amount of time the product remains at the final temperature, after it has been removed from a grill, oven, or other heat source. During the three minutes after meat is removed from the heat source, its temperature remains constant or continues to rise, which destroys pathogens."

    For more information view the source:Center for Disease Control

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  • TREMATODES

    Trematodes

    Definition: Trematoda is a class within the phylum Platyhelminthes that contains two groups of parasitic flatworms, commonly referred to as "flukes".


    For more information view the source:Wikipedia

     

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  • TRICHOSTRONGYLUS

    Trichostrongylus species are nematodes (round worms), which are ubiquitous among herbivores worldwide, including cattle, sheep, donkeys, goats, deer, and rabbits . At least 10 Trichostrongylus species have been associated with human infections. Infections occur via ingestion of infective larvae from contaminated vegetables or water . Epidemiological studies indicate a worldwide distribution of Trichostrongylus infections in humans, with the highest prevalence rates observed in individuals from regions with poor sanitary conditions, in rural areas, or who are farmers / herders. Human infections are most prevalent in the Middle East and Asia , with a worldwide estimated prevalence of 5.5 million. 

     

    CLINICAL PRESENTATION

    The majority of human infections are asymptomatic or associated with mild symptoms. Symptomatic individuals may experience abdominal pain, nausea, diarrhea, flatulence, dizziness, generalized fatigue, and malaise. Eosinophilia is frequently observed. Infections with a heavy worm burden can lead to anemia, cholecystitis, and emaciation. 

     

    DIAGNOSIS

    The adult worms live in the small intestine. The diagnosis is based on the observation of eggs in the stool. The eggs are 85-115 um, oval, elongated, and pointed at one or both ends. Trichostrongylus eggs must be differentiated from hookworm eggs which are smaller and do not have pointed ends. 

     

    PREVENTION AND TREATMENT

    Since the use of herbivore manure as fertilizer is a common practice preceding infection, thorough cleaning and cooking of vegetables is required for prevention of infection. Treatment with pyrantel pamoate (11 mg/kg base once, max. 1 g) is recommended. Alternative agents include mebendazole (100 mg bid x 3 days) and albendazole (400 mg once).Successful treatment with ivermectin has also been reported.

     

    Egg of Trichostrongylus sp.

    For more information view the source:Wikipedia

     

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  • TRICHURIS TRICHIURA

    An estimated 604-795 million people in the world are infected with whipworm. Whipworm, hookworm, and Ascaris are known as soil-transmitted helminths (parasitic worms). Together, they account for a major burden of disease worldwide.  Whipworms live in the large intestine and whipworm eggs are passed in the feces of infected persons. If the infected person defecates outside (near bushes, in a garden, or field) or if human feces as used as fertilizer, eggs are deposited on soil. They can then mature into a form that is infective. Whipworm infection is caused by ingesting eggs. This can happen when hands or fingers that have contaminated dirt on them are put in the mouth or by consuming vegetables or fruits that have not been carefully cooked, washed or peeled.  People infected with whipworm can suffer light or heavy infections. People with light infections usually have no symptoms. People with heavy symptoms can experience frequent, painful passage of stool that contains a mixture of mucus, water, and blood. Rectal prolapse can also occur. Children with heavy infections can become severely anemic and growth-retarded. Whipworm infections are treatable with medication prescribed by your health care provider.

     

    FAQS

    What is whipworm?

    Whipworm (Trichuris trichiura)  is an intestinal parasite of humans. The larvae and adult worms live in the  intestine of humans and can cause intestinal disease. The name is derived from the worm’s  distinctive whip-like shape.

    How is whipworm spread?

    Whipworms live in the intestine and whipworm eggs are passed  in the feces of infected persons. If the  infected person defecates outside (near bushes, in a garden, or field), or if  the feces of an infected person are used as fertilizer, then eggs are deposited  on the soil. They can then mature into a  form that is infective. Roundworm  infection is caused by ingesting eggs. This can happen when hands or fingers that have contaminated dirt on  them are put in the mouth, or by consuming vegetables or fruits that have not  been carefully cooked, washed or peeled.

    Who is at risk for infection?

    Infection occurs worldwide in warm and humid climates where sanitation  and hygiene are poor, including in temperate climates during warmer  months. Persons in these areas are at  risk if soil contaminated with human feces enters their mouths or if they eat  vegetables or fruits that have not been carefully washed, peeled or cooked.

    What are the signs and symptoms of whipworm?

    People with light infections usually have no signs or symptoms. People with  heavy infections can experience frequent, painful passage of stool that contains  a mixture of mucus, water, and blood. The diarrhea typically has an acrid smell. In severe cases growth retardation can  occur. Rectal prolapse can also  occur. In children, heavy infection may be associated with growth retardation and impaired cognitive development.

    How is whipworm diagnosed?

    Health  care providers can diagnose whipworm by taking a stool sample. By using a microscope, providers can look for  the presence of whipworm eggs.

    How can I prevent infection?

    • Avoid contact with soil that may be contaminated with human feces, including with human fecal matter ("night soil") used to  fertilize crops.
    • Wash your hands with soap and warm water before handling food.
    • Teach children the importance of washing hands to prevent infection.
    • Wash, peel, or cook all raw vegetables and fruits before eating, particularly those that have been grown in soil that has been fertilized with manure.

    Transmission of infection to others can be prevented by:

    • not defecating outdoors, and by
    • effective sewage disposal systems.

    What is the treatment for whipworm?

    Whipworm infections are generally treated for 1-3 days with medication  prescribed by your health care provider. The drugs are effective and appear to have few side effects.

    What is preventive treatment?

    In developing countries, groups at higher risk for soil-transmitted  helminth infections (hookworm, Ascaris, and whipworm) are often treated  without a prior stool examination. Treating in this way is called preventive treatment (or "preventive  chemotherapy"). The high-risk groups identified by the World Health Organization are preschool and school-age children, women of childbearing age  (including pregnant women in the 2nd and 3rd trimesters  and lactating women) and adults in occupations where there is a high risk of  heavy infections. School-age children  are often treated through school-health programs and preschool children and  pregnant women at visits to health clinics.

    What is mass drug administration (MDA)?

    The soil-transmitted helminths (hookworm, Ascaris, and whipworm) and  four other "neglected tropical diseases" (river blindness, lymphatic  filariasis, schistosomiasis and trachoma) are sometimes treated through mass drug  administrations. Since the drugs used  are safe and inexpensive or donated, entire risk groups are offered preventive  treatment. Mass drug administrations are  conducted periodically (often annually), commonly with drug distributors who go door-to-door. Multiple neglected tropical diseases are often treated simultaneously using MDAs.

     

    EPIDEMIOLOGY & RISK FACTORS

    Whipworm is a soil-transmitted helminth (STH) and is the third most  common roundworm of humans. Whipworm  causes an infection called trichuriasis and often occurs in areas where human  feces is used as fertilizer or where defecation onto soil happens. The worms are spread from person to person by  fecal-oral transmission or through feces-contaminated food.

     

    GEOGRAPHIC DISTRIBUTION

    Worldwide, infection occurs more frequently in areas with tropical  weather and poor sanitation practices, and among children. In 2002, the estimated number of persons  infected with whipworm was 1 billion. Trichuriasis also occurs in the southern United States.

     

    BIOLOGY

    Causal Agent:

    The nematode (roundworm) Trichuris trichiura, also called the human whipworm

     

    Life Cycle:

    Life Cycle of Strongyloides

    The unembryonated eggs are passed with the stool. In the soil, the eggs develop into a 2-cell stage, an advanced cleavage stage, and then they embryonate;  eggs become infective in 15 to 30 days. After ingestion  (soil-contaminated hands or food), the eggs hatch in the small  intestine, and release larvae that mature and establish themselves as adults in the colon. The adult worms (approximately 4 cm in length) live in the cecum and ascending colon. The adult worms are fixed in that location, with the anterior portions threaded into the mucosa. The females begin to oviposit 60 to 70 days after infection. Female worms in the cecum shed between 3,000 and 20,000 eggs per day. The life span of the adults is about 1 year.

    Life cycle image and information courtesy of DPDx.

     

    DISEASE

    People infected with whipworm can suffer light or heavy  infections. People with light infections  usually have no symptoms. People with  heavy symptoms can experience frequent, painful passage of stool that contains  a mixture of mucus, water, and blood. Rectal prolapse can also occur. Heavy infection in children can lead to severe anemia, growth retardation, and impaired cognitive development. Whipworm infections are treatable with medication prescribed by your health care provider.

     

    DIAGNOSIS

    The standard method for diagnosing the presence of whipworm is by microscopically  identifying whipworm eggs in a stool sample. Because eggs may be difficult to find in light infections, a  concentration procedure is recommended.

     

    PREVENTION AND CONTROL

    The best way to prevent whipworm infection is to always:    

    • Avoid ingesting soil that may be contaminated  with human feces, including where human fecal matter ("night soil") or  wastewater is used to fertilize crops.
    • Wash your hands with soap and warm water before handling food.
    • Teach children the importance of washing hands to prevent infection.
    • Wash, peel, or cook all raw vegetables and  fruits before eating, particularly those that have been grown in soil that has  been fertilized with manure.

    Transmission of infection to others can be prevented by:    

    • Not defecating  outdoors.
    • Effective sewage  disposal systems.

    For more information view the source:Center for Disease Control

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  • TRYPANOSOMA

    Trypanosoma is a genus of kinetoplastids (class Kinetoplastida), a monophyletic group of unicellular parasitic flagellate protozoa. The name is derived from the Greek trypano (borer) and soma (body) because of their corkscrew-like motion. All trypanosomes are heteroxenous (requiring more than one obligatory host to complete life cycle) and are transmitted via a vector. The majority of species are transmitted by blood-feeding invertebrates, but there are different mechanisms among the varying species. Then in the invertebrate host they are generally found in the intestine and normally occupy the bloodstream or an intracellular environment in the mammalian host. Trypanosomes infect a variety of hosts and cause various diseases, including the fatal human diseases sleeping sickness, caused by Trypanosoma brucei, and Chagas disease, caused by Trypanosoma cruzi. The mitochondrial genome of the Trypanosoma, as well as of other kinetoplastids, known as the kinetoplast, is made up of a highly complex series of catenated circles and minicircles and requires a cohort of proteins for organisation during cell division.

     

    HISTORY

    The first species of Trypanosoma identified was in a trout by Valentin in 1841. They were identified in mammals 25-30 years later.

    HOSTS, LIFE CYCLE AND MORPHOLOGIES

    Two different types of trypanosomes exist, and their life cycles are different, the salivarian species and the stercorarian species. Stercorarian trypanosomes infect the insect, most often the triatomid kissing bug, develop in its posterior gut and infective organisms are released in the faeces and deposited on the skin of the host. The organism then penetrates and can disseminate throughout the body. Insects become infected when taking a blood meal. Salivarian trypanosomes develop in the anterior gut of insects, most importantly the Tsetse fly, and infective organisms are inoculated into the host by the insect bite before it feeds. As trypanosomes progress through their life cycle they undergo a series of morphological changes as is typical of trypanosomatids. The life cycle often consists of the trypomastigote form in the vertebrate host and the trypomastigote or promastigote form in the gut of the invertebrate host. Intracellular lifecycle stages are normally found in the amastigote form. The trypomastigote morphology is unique to species in the genus Trypanosoma.

    For more information view the source:Wikipedia

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  • TRYPANOSOMIASIS

    Trypanosoma is a genus of kinetoplastids (class Kinetoplastida), a monophyletic group of unicellular parasitic flagellate protozoa. The name is derived from the Greek trypano (borer) and soma (body) because of their corkscrew-like motion. All trypanosomes are heteroxenous (requiring more than one obligatory host to complete life cycle) and most are transmitted via a vector. The majority of species are transmitted by blood-feeding invertebrates, but there are different mechanisms among the varying species. Then in the invertebrate host they are generally found in the intestine and normally occupy the bloodstream or an intracellular environment in the mammalian host.  Trypanosomes infect a variety of hosts and cause various diseases, including the fatal human diseases sleeping sickness, caused by Trypanosoma brucei, and Chagas disease, caused by Trypanosoma cruzi.  The mitochondrial genome of the Trypanosoma, as well as of other kinetoplastids, known as the kinetoplast, is made up of a highly complex series of catenated circles and minicircles and requires a cohort of proteins for organisation during cell division.

     

    BIOLOGY

    CAUSAL AGENTS

    The protozoan parasite, Trypanosoma cruzi, causes Chagas disease, a zoonotic disease that can be transmitted to humans by blood-sucking triatomine bugs.  To see drawings of some common species of triatomine bugs found in the United States.

     

    LIFE CYCLE

     

    Life cycle of Trypanosma cruzi

    An infected triatomine insect vector (or “kissing” bug) takes a blood meal and releases trypomastigotes in its feces near the site of the bite wound.  Trypomastigotes enter the host through the wound or through intact mucosal membranes, such as the conjunctiva .  Common triatomine vector species for trypanosomiasis belong to the genera Triatoma, Rhodnius, and Panstrongylus.  Inside the host, the trypomastigotes invade cells near the site of inoculation, where they differentiate into intracellular amastigotes .  The amastigotes multiply by binary fission  and differentiate into trypomastigotes, and then are released into the circulation as bloodstream trypomastigotes .  Trypomastigotes infect cells from a variety of tissues and transform into intracellular amastigotes in new infection sites.  Clinical manifestations can result from this infective cycle.  The bloodstream trypomastigotes do not replicate (different from the African trypanosomes).  Replication resumes only when the parasites enter another cell or are ingested by another vector.  The “kissing” bug becomes infected by feeding on human or animal blood that contains circulating parasites .  The ingested trypomastigotes transform into epimastigotes in the vector’s midgut .  The parasites multiply and differentiate in the midgut  and differentiate into infective metacyclic trypomastigotes in the hindgut . Trypanosoma cruzi can also be transmitted through blood transfusions, organ transplantation, transplacentally, and in laboratory accidents.

     

    GEOGRAPHIC DISTRIBUTION

    The Americas from the southern United States to southern Argentina.  Mostly in poor, rural areas of Mexico, Central America, and South America.  Chronic Chagas disease is a major health problem in many Latin American countries. 

     

    CLINICAL FEATURES

    The acute phase is usually asymptomatic, but can present with manifestations that include fever, anorexia, lymphadenopathy, mild hepatosplenomegaly, and myocarditis.  Romańa's sign (unilateral palpebral and periocular swelling) may appear as a result of conjunctival contamination with the vector's feces.  A nodular lesion or furuncle, usually called chagoma, can appear at the site of inoculation.  Most acute cases resolve over a period of a few weeks or months into an asymptomatic chronic form of the disease.  The symptomatic chronic form may not occur for years or even decades after initial infection.  Its manifestations include cardiomyopathy (the most serious manifestation); pathologies of the digestive tract such as megaesophagus and megacolon; and weight loss.  Chronic Chagas disease and its complications can be fatal.

     

    LABORATORY DIAGNOSIS

    Demonstration of the causal agent is the diagnostic procedure in acute Chagas disease.  It almost always yields positive results, and can be achieved by: Microscopic examination: a) of fresh anticoagulated blood, or its buffy coat, for motile parasites; and b) of thin and thick blood smears stained with Giemsa, for visualization of parasites. Isolation of the agent: a) inoculation in culture with specialized media (e.g. NNN, LIT); b) inoculation into mice; and c) xenodiagnosis, where uninfected triatomine bugs are fed on the patient's blood, and their gut contents examined for parasites 4 weeks later. 

    For more information view the source:Center for Disease Control

     

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  • WUCHERERIA

    Wuchereria bancrofti is a parasitic filarial nematode (roundworm) spread by a mosquito vector. It is one of the three parasites that cause lymphatic filariasis, an infection of the lymphatic system by filarial worms. It affects over 120 million people, primarily in Africa, South America, and other tropical and subtropical countries. If the infection is left untreated, it can develop into a chronic disease called elephantiasis. Limited treatment modalities exist and no vaccines have been developed.

     

    BIOLOGY

    CAUSAL AGENTS

    Filariasis is caused by nematodes (roundworms) that inhabit the lymphatics and subcutaneous tissues.  Eight main species infect humans.  Three of these are responsible for most of the morbidity due to filariasis: Wuchereria bancrofti and Brugia malayi cause lymphatic filariasis, and Onchocerca volvulus causes onchocerciasis (river blindness).  The other five species are Loa loa, Mansonella perstans, M. streptocerca, M. ozzardi, and Brugia timori.  (The last species also causes lymphatic filariasis.)

     

    LIFE CYCLE

    Infective larvae are transmitted by infected biting arthropods during a blood meal.  The larvae migrate to the appropriate site of the host's body, where they develop into microfilariae-producing adults.  The adults dwell in various human tissues where they can live for several years.  The agents of lymphatic filariasis reside in lymphatic vessels and lymph nodes; Onchocerca volvulus in nodules in subcutaneous tissues; Loa loa in subcutaneous tissues, where it migrates actively; Brugia malayi in lymphatics, as with Wuchereria bancrofti; Mansonella streptocerca in the dermis and subcutaneous tissue; Mansonella ozzardi apparently in the subcutaneous tissues; and M. perstans in body cavities and the surrounding tissues.  The female worms produce microfilariae which circulate in the blood, except for those of Onchocerca volvulus and Mansonella streptocerca, which are found in the skin, and O. volvulus which invade the eye.  The microfilariae infect biting arthropods (mosquitoes for the agents of lymphatic filariasis; blackflies [Simulium] for Onchocerca volvulus; midges for Mansonella perstans and M. streptocerca; and both midges and blackflies for Mansonella ozzardi; and deerflies [Chrysops] for Loa loa).  Inside the arthropod, the microfilariae develop in 1 to 2 weeks into infective filariform (third-stage) larvae.  During a subsequent blood meal by the insect, the larvae infect the vertebrate host.  They migrate to the appropriate site of the host's body, where they develop into adults, a slow process than can require up to 18 months in the case of Onchocerca.

     

    LIFE CYCLE OF WUCHERERIA BANCROFTI

    Life cycle of Wuchereria bancrofti

    Different species of the following genera of mosquitoes are vectors of W. bancrofti filariasis depending on geographical distribution.  Among them are: Culex (C. annulirostris, C. bitaeniorhynchus, C. quinquefasciatus, and C. pipiens); Anopheles (A. arabinensis, A. bancroftii, A. farauti, A. funestus, A. gambiae, A. koliensis, A. melas, A. merus, A. punctulatus and A. wellcomei); Aedes (A. aegypti, A. aquasalis, A. bellator, A. cooki, A. darlingi, A. kochi, A. polynesiensis, A. pseudoscutellaris, A. rotumae, A. scapularis, and A. vigilax); Mansonia (M. pseudotitillans, M. uniformis); Coquillettidia (C. juxtamansonia).  During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound .  They develop in adults that commonly reside in the lymphatics .  The female worms measure 80 to 100 mm in length and 0.24 to 0.30 mm in diameter, while the males measure about 40 mm by .1 mm.  Adults produce microfilariae measuring 244 to 296 um by 7.5 to 10 um, which are sheathed and have nocturnal periodicity, except the South Pacific microfilariae which have the absence of marked periodicity.  The microfilariae migrate into lymph and blood channels moving actively through lymph and blood .  A mosquito ingests the microfilariae during a blood meal .  After ingestion, the microfilariae lose their sheaths and some of them work their way through the wall of the proventriculus and cardiac portion of the mosquito's midgut and reach the thoracic muscles .  There the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae .  The third-stage infective larvae migrate through the hemocoel to the mosquito's prosbocis  and can infect another human when the mosquito takes a blood meal.

     

    GEOGRAPHIC DISTRIBUTION

    Among the agents of lymphatic filariasis, Wuchereria bancrofti is encountered in tropical areas worldwide; Brugia malayi is limited to Asia; and Brugia timori is restricted to some islands of Indonesia.  The agent of river blindness, Onchocerca volvulus, occurs mainly in Africa, with additional foci in Latin America and the Middle East.  Among the other species, Loa loa and Mansonella streptocerca are found in Africa; Mansonella perstans occurs in both Africa and South America; and Mansonella ozzardi occurs only ins the Americas, from Mexico south to South America and in the Caribbean. 

     

    CLINICAL FEATURES

    Most infections are probably asymptomatic, as indicated by serologic surveys.  Manifestations of disease include fever, chills, sweating, myalgias, fatigue, hepatosplenomegaly, and hemolytic anemia.  Symptoms typically occur after an incubation period of 1 to 4 weeks, and can last several weeks.  The disease is more severe in patients who are immunosuppressed, splenectomized, and/or elderly.  Infections caused by B. divergens tend to be more severe (frequently fatal if not appropriately treated) than those due to B. microti, where clinical recovery usually occurs.

     

    LABORATORY DIAGNOSIS

    Identification of microfilariae by microscopic examination is the most practical diagnostic procedure. Examination of blood samples will allow identification of microfilariae of Wuchereria bancrofti, Brugia malayi, Brugia timori, Loa loa, Mansonella perstans, and M. ozzardi.  It is important to time the blood collection with the known periodicity of the microfilariae.  The blood sample can be a thick smear, stained with Giemsa or hematoxylin and eosin.  For increased sensitivity, concentration techniques can be used.  These include centrifugation of the blood sample lyzed in 2% formalin (Knott's technique), or filtration through a Nucleopore® membrane. Examination of skin snips will identify microfilariae of Onchocerca volvulus and Mansonella streptocerca.  Skin snips can be obtained using a corneal-scleral punch, or more simply a scalpel and needle.  The sample must be allowed to incubate for 30 minutes to 2 hours in saline or culture medium, and then examined for microfilariae that would have migrated from the tissue to the liquid phase of the specimen.

    For more information view the source:Center for Disease Control

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